Gotowe bibliografie tematyczne / Cox

Gotowa bibliografia na temat „Cox”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 1 sierpnia 2024

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Artykuły w czasopismach na temat "Cox"

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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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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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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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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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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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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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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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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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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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Rozprawy doktorskie na temat "Cox"

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Dario, Alan de Genaro. "Processos de Cox com intensidade difusiva afim". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/45/45133/tde-01052013-111713/.

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Esta Tese explora o Processo de Cox quando sua intensidade pertence a uma família de difusões afim. A forma da funçâo densidade de Probabilidade do Processo de Cox é obtida quando a intensidade é descrita por uma difusão fim d-dimensional arbitrária. Analisa-se também o acoplamento e convergência para o Processo de Cox com intensidade afim. Para ilustrar assume-se que a intensidade do Processo é governada por uma difusão de Feller e resultados mais detalhados são obtidos. Adicionalmente, os parâmetros da intensidade do Processo são estimados por meio do Filtro de Kalman conjugado com o estimador de Quase-Máxima Verossimilhança.
This Thesis deals with the Cox Process when its intensity belongs to a family of affine diffusions. The form of the probability density function of the Cox process is obtained when the density is described by an arbitrary d-dimensional affine diffusion. Coupling and convergence results are also addressed for a general Cox process with affine intensity. We adopted the Feller diffusion for driving the underlying intensity of the Cox Process to illustrate our results. Additionally the parameters of the underlying intensity processes are estimated by means of the Kalman Filter in conjunction with Quasi-Maximum Likelihood estimation.
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Cox, Benjamin Samuel. "Assessment of an invasive lake trout population in Swan Lake, Montana". Thesis, Montana State University, 2010. http://etd.lib.montana.edu/etd/2010/cox/CoxB0810.pdf.

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The recent invasion of lake trout into the Swan River drainage in Northwest Montana threatens one of the last remaining recreational bull trout fisheries in the USA. An inter-agency group is implementing an experimental lake trout suppression program on Swan Lake. The objectives of this study were to establish a baseline data set on the lake trout population in Swan Lake concurrently with the experimental removal effort, simulate alternative management scenarios using matrix models and identify spawning locations of lake trout to target adult fish and embryos. A commercial gill-net sampling effort provided data to estimate abundance, size structure, age structure, growth, condition, maturity, fecundity, and mortality of lake trout in Swan Lake. Lake trout in Swan Lake grew rapidly, attained large sizes, and were in high condition. The size and age structure of lake trout sampled was skewed towards juvenile lake trout, indicating the population was growing rapidly. Matrix-model simulations also indicated the lake trout population would continue to grow with no suppression efforts, but suppression efforts could reduce the population growth rate. Population growth was particularly sensitive to changes in age-0 survival in population models. Elasticity analysis of matrix simulations indicated survival from birth to sexual maturity, followed by survival of adult fish contributed most to population growth. Lake trout spawning locations were identified using ultrasonic telemetry, short-set gill nets, and in-situ egg nets. Spawning locations identified with acoustic telemetry were confirmed by capturing gravid lake trout in gill nets and lake trout eggs in the substrate. These results suggest that the inter-agency group should focus removal efforts on sub-adult and adult lake trout at if extirpation of the population is the goal. Given the uncertainty in the vital rates and the potential bias in exploitation rates used to model suppression scenarios, annual suppression efforts should be increased from the 2008 level to ensure a decline in the lake trout population.
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Martinez, Ruiz Roxana de Jesus, i Rojas Juan Pablo Gomez. "“EFECTIVIDAD DE LA ANALGESIA EN POSOPERADAS DE CESAREA CON TRAMADOL PERIDURAL ASOCIADO A: KETOROLACO IV (COX-1) vs DICLOFENACO IV (COX-2) vs PARACETAMOL IV (COX-3) IV”". Tesis de Licenciatura, Medicina-Quimica, 2014. http://ri.uaemex.mx/handle/123456789/14614.

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De, la Puente Candamo ED José Agustín. "Josefina Ramos de Cox". Pontificia Universidad Católica del Perú, 2014. http://repositorio.pucp.edu.pe/index/handle/123456789/114442.

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Sun, Haipeng. "Regulation of Cyclooxygenase Gene Expression by Glucocorticoids in Cardiomyocytes". Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/194896.

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Glucocorticoids (GCs) are endogenous steroid hormones that regulate a number of critical physiological processes. Psychological stress increases the level of GCs in the circulating system. The biological effect of elevated GCs on the heart is not well understood. We found that GCs induced Cyclooxygenase-1 (COX-1) and COX-2 gene expression in cardiomyocytes. COX-1 or COX-2 encodes the rate-limiting enzyme in the biosynthesis of prostanoids, which modulate crucial physiological and pathophysiological responses. The present studies aim to elucidate the signaling transduction pathway and the mechanism underlying GC induced COX expression.Our data demonstrate that GCs activate COX-1 gene expression through transcriptional regulation. COX-1 gene promoter studies support a role of Sp binding site in CT induced COX-1 gene expression. The nuclear protein binding to this site appears to be Sp3 transcription factor. Co-immunoprecipitation assays indicated a physical interaction between GR and Sp3 protein. Silencing of Sp3 transcription factor with small interfering RNA suppressed CT-induced COX-1 promoter activation. These data suggest that the activated GR interacts with Sp3 transcription factor that binds to COX-1 promoter to up-regulate COX-1 gene expression in cardiomyocytes.We also found that administration of GC in adult mice increased the level of COX-2 in the ventricles. With isolated neonatal cardiomyocytes, corticosterone (CT) induces the transcription of COX-2 gene. This response appears to be cardiomyocyte cell type specific and GC receptor (GR)-dependent. CT causes activation of p38 MAPK and subsequently CREB phosphorylation that mediates COX-2 gene expression. Mifepristone, a GR antagonist, failed to inhibit p38 and CREB activation and p38 inhibition failed to prevent activation of GR. These data suggest that two parallel signaling pathways, GR and p38 MAPK, act in concert to regulate the expression of COX-2 gene in cardiomyocytes.In addition to the investigation of mechanism and signaling transduction pathway, I have explored pharmacological agents that modulate COX expression. LY294002, a commonly used PI3K inhibitor, inhibited COX-2 gene expression via a PI3K-independent mechanism. Whereas GSK-3 inhibitors, such as lithium chloride, upregulated COX-2 gene expression, but suppressed GC-induced COX-1 expression. These data have paved the foundation for pharmacological manipulation of COX-1 and COX-2 gene expression in the heart.
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Noppakaew, Passawan. "Parabolic projection and generalized Cox configurations". Thesis, University of Bath, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.642047.

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Building on the work of Longuet-Higgins in 1972 and Calderbank and Macpherson in 2009, we study the combinatorics of symmetric configurations of hyperplanes and points in projective space, called generalized Cox configurations. To do so, we use the formalism of morphisms between incidence systems. We notice that the combinatorics of Cox configurations are closely related to incidence systems associated to certain Coxeter groups. Furthermore, the incidence geometry of projective space P (V ), where V is a vector space, can be viewed as an incidence system of maximal parabolic subalgebras in a semisimple Lie algebra g, in the special case g = pgl (V ) the projective general linear Lie algebra of V . Using Lie theory, the Coxeter incidence system for the Coxeter group, whose Coxeter diagram is the underlying diagram of the Dynkin diagram of the g, can be embedded into the parabolic incidence system for g. This embedding gives a symmetric geometric configuration which we call a standard parabolic configuration of g. In order to construct a generalized Cox configuration, we project a standard parabolic configuration of type Dn into the parabolic incidence system of projective space using a process called parabolic projection, which maps a parabolic subalgebra of the Lie algebra to a parabolic subalgebra of a lower dimensional Lie algebra. As a consequence of this construction, we obtain Cox configurations and their analogues in higher dimensional projective spaces. We conjecture that the generalized Cox configurations we construct using parabolic projection are nondegenerate and, furthermore, any non-degenerate Cox configuration is obtained in this way. This conjecture yields a formula for the dimension of the space of non-degenerate generalized Cox configurations of a fixed type, which enables us to develop a recursive construction for them. This construction is closely related to Longuet-Higgins’ recursive construction of (generalized) Clifford configurations but our examples are more general and involve the extra parameters.
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Beyan, Huriya. "Altered monocyte cox-1 & cox-2 levels in human type 1 diabetes". Thesis, Queen Mary, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408256.

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Wright, William. "Investigating the role of COX-1 and COX-2 in Toll-Like Receptor responses". Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24789.

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COX is the rate-limiting enzyme in the conversion of arachidonic acid to the prostanoids. It is present in humans as two isoforms, COX-1 and COX-2. COX-1 is constitutively expressed and involved in homeostatic functions, while COX-2 expression is mostly limited to sites of inflammation. The precise function of COX isoforms is a subject of debate, particularly with respect to nonsterodial anti-inflammatory drug (NSAID)-induced toxicity. Toll-like receptors (TLRs) trigger the immune response following recognition of pathogen-associated molecular patterns (PAMPs), such as bacterial lipopolysaccharide (LPS), which activates TLR4. The role of COX-1 and COX-2 in responses to different TLRs is incompletely understood. The main focus of my PhD was to investigate COX-1 and COX-2 function in innate immunity, using TLR agonists in mice lacking COX-1 or COX-2. I also studied this in relation to lung inflammation using lung fibroblasts, and isolated pulmonary arteries to examine the effect of prostanoids on pulmonary vascular responses. Lung fibroblasts isolated from COX-2-/- mice were more proliferative than lung fibroblasts from wild-type or COX-1-/- mice. They also released greater amounts of cytokines when stimulated with various TLR agonists. Human lung fibroblasts were particularly sensitive to TLR3 agonists, and cytokine release was enhanced in the presence of NSAIDs. The effect of diclofenac may have been caused by inhibition of COX-related prostaglandin (PG) E2. In in vivo studies, Cox2 gene expression was strongly induced by TLR4 activation in all organs and less so by TLR3 activation, where induction was restricted to the spleen and stomach. Mice lacking COX-2 released higher amounts of anti-viral proteins following TLR3 activation with poly (I:C). This suggests that COX-2-specific NSAIDs may boost the anti-viral response, thus proving beneficial over traditional NSAIDs during viral infection. In the pulmonary vasculature, I found that most prostacyclin drugs were limited by actions on EP3 receptors, but that selective peroxisome proliferator-activated receptor (PPAR)β/δ agonists were active as dilators under all conditions. Deletion of COX-1 or COX-2 affected the ability of mouse pulmonary arteries to release endothelial-derived nitric oxide but not to respond to IP or PPARβ/δ agonists. Finally, activation of adenosine monophosphate kinase (AMPK) had no direct dilator effect on pulmonary vessels. However, preliminary data suggest that pretreatment of vessels with an AMPK activator enhanced (additive) dilation induced by PPARβ/δ, indicating a potential benefit in pulmonary arterial hypertension (PAH). In summary, my in vitro and in vivo experiments using mice lacking COX-1 or COX-2 provide insight into the role of COX in immunity and the pulmonary vasculature.
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Franco, del Pino David. "Modulación serotonérgica de inhibidores de COX-1 y COX-2 en dolor agudo experimental". Tesis, Universidad de Chile, 2006. http://repositorio.uchile.cl/handle/2250/140302.

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Trabajo de Investigación Requisito para optar al Título de Cirujano Dentista
El dolor es la primera causa de consulta al odontólogo. Por esto que es de suma importancia saber tratarlo correctamente para poder brindar a nuestros pacientes una solución eficaz a su problema. En las últimas décadas se ha centrado el estudio del dolor en animales mediante el uso de métodos algesiométricos que permitan evaluar el efecto antinociceptivo de distintos fármacos analgésicos y sus combinaciones. Un grupo de éstos son los analgésicos antiinflamatorios no esteroidales (AINEs) los cuales son ampliamente utilizados en el dolor; sin embargo, su uso conlleva una serie de efectos adversos que limitan su uso. Para contrarrestarlos, se están desarrollando combinaciones de fármacos que permitan aumentar los efectos analgésicos y disminuir las reacciones adversas. En este trabajo de investigación, se estudio la interacción analgésica de la coadministración de ketorolaco y meloxicam en el test de las contorsiones abdominales inducidas por ácido acético y la participación del sistema serotonérgico en dicha interacción. Se usaron ratones de la cepa CF- 1, a los que se les administró vía intraperitoneal 1/2, 1/4, 1/8, 1/16 de las DE50 de la combinación ketorolaco / meloxicam y por medio de análisis isobolográfico se determinó que la interacción, resultó ser sinérgica o supraaditiva. El pretratamiento con tropisetrón 1mg/kg (i.p.), antagonista selectivo de receptores de serotonina del subtipo 5HT-3, no modificó la naturaleza de la interacción, lo que pone en evidencia que la participación del sistema serotonérgico a través de estos receptores no participa significativamente, en el mecanismo de acción de la combinación ketorolaco / meloxicam.
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Ghassani, Mohamad. "Dynamiques épidémiques, risques et copules". Thesis, Grenoble, 2012. http://www.theses.fr/2012GRENS027/document.

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Les modèles stochastiques classiques comportent des copules d'interactions linéaires, exprimant en général des interactions de paire. Il sera envisagé d'étendre ces modèles à des interactions non linéaires de type saturation ou de type triplet, en vue de traiter des applications réalistes, comme les diffusions épidémiques.Le but de cette thèse est d'introduire les fonctions copules en épidémiologie, et surtout d'appliquer ces fonctions sur le système de transmission de la Malaria afin de constater la dépendance entre les différents compartiments du système. Nous étudierons quelques modèles compartimentaux, qui sont une généralisation du modèle de Ross-Macdonald, en supposant que la population n'est pas constante et en prenant en compte des paramètres de transmission comme la fécondité, la mortalité et autres. Aussi, nous introduirons les classes d'âges dans certains de ces modèles compartimentaux, afin de trouver une relation entre les individus de ces classes d'âges à l'aide du modèle de Cox et des fonctions copules. Nous donnerons ensuite, deux exemples sur ces modèles : la Malaria au Mali et la peste en Europe au moyen-âge. Nous introduirons aussi les quantiles conditionnels et les fonctions copules archimédiennes, ce qui nous mènera à trouver une dépendance entre les différents compartiments des hôtes et des vecteurs
The stochastic classical models include linear interactions copulas, expressing in general pair interactions. It is planned to extend these models to nonlinear interactions of saturation type or triplet type, to treat realistic applications, as the epidemics diffusions.The aim of this thesis is to apply the copulas functions in epidemiology, and especially to apply these functions in the transmission system of malaria to detect the dependence existing between compartments of the epidemic system. We will study some compartmental models, which are a generalization of the Ross-Macdonald model, assuming that the population is not constant and taking into account the transmission parameters such as fertility, mortality, etc. Also, we will introduce the age classes in some of these compartmental models, and study the relationships between individuals of these age classes, using the Cox model and the copulas functions. Then, we will give two examples of these models: the Malaria in Mali and the plague in Europe during the Middle Ages. We will introduce also the conditional quantiles and the Archimedean copulas functions, that will lead us to find dependencies between the different compartments of hosts and vectors
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Książki na temat "Cox"

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Lace, Kate. Cox. London: CArrow, 2012.

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(Firm), Cox &. Power. Cox & Power. London: Cox & Power, 1995.

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Franck, Mallet, red. Paul Cox. Paris: Pyramyd, 2003.

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Copyright Paperback Collection (Library of Congress), red. Elaine Cox. New York, NY: Blue Moon, 2001.

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Gallery, Tate, red. Stephen Cox. London: Tate Gallery Publications, 1986.

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Chetwin, Grace. Box and Cox. New York: Bradbury Press, 1990.

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Pairet, Michel, i Joanne van Ryn, red. COX-2 Inhibitors. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7879-1.

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Warner, Yvonne Story. The family Cox. [Vienna, Va.] (2433 McClintic Court, Vienna 22180): Y.S. Warner, 1987.

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Stephen, Cox. Stephen Cox: Scultura. Firenze: Galleria Carini, 1987.

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Michaels, Myerna. The Cox family. Redaktorzy Brady Peg 1920-, Kaiser Sina 1927- i Cox James Henry 1935-. Syracuse, IN: Distributed to all living descendants of Azro Loyd and Bianca Bell Sina Cox by James Henry Cox, 2004.

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Części książek na temat "Cox"

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Grandell, Jan. "Cox models". W Springer Series in Statistics, 77–124. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4613-9058-9_4.

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Juhász-Ormsby, Ágnes. "Cox, Leonard". W Encyclopedia of Renaissance Philosophy, 1–6. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-02848-4_478-1.

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Juhász-Ormsby, Ágnes. "Cox, Leonard". W Encyclopedia of Renaissance Philosophy, 901–6. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-14169-5_478.

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Salajegheh, Ali. "COX 10". W Angiogenesis in Health, Disease and Malignancy, 51–54. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_10.

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Hanson, R. Karl. "Cox regression." W Prediction statistics for psychological assessment., 177–93. Washington: American Psychological Association, 2022. http://dx.doi.org/10.1037/0000275-010.

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Phelps, Hollis. "Harvey Cox". W The Palgrave Handbook of Radical Theology, 117–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96595-6_8.

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Peters, Nils, Martin Dichgans, Sankar Surendran, Josep M. Argilés, Francisco J. López-Soriano, Sílvia Busquets, Klaus Dittmann i in. "COX Deficiency". W Encyclopedia of Molecular Mechanisms of Disease, 458. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8290.

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Cleophas, Ton J., i Aeilko H. Zwinderman. "Cox Regressions". W Modern Survival Analysis in Clinical Research, 9–15. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-31632-6_2.

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Cao, Mingqin. "Cox Regression". W Textbook of Medical Statistics, 209–20. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-7390-3_15.

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Dixon, D. A. "Regulation of COX-2 Expression in Human Cancers". W COX-2, 52–71. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071363.

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Streszczenia konferencji na temat "Cox"

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Shao, W., C. Kuhn, D. Mayr, N. Ditsch, S. Mahner, N. Harbeck, V. Cavaillès, U. Jeschke i S. Sixou. "Untersuchungen zur differenzierten Expression von PPARγ, Cox-1 und Cox-2 beim Mammakarzinom". W Abstracts zum Kongress 2019 der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde (BGGF) und der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1693862.

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Tribus, Myron. "An appreciation of Richard Threlkeld Cox". W BAYESIAN INFERENCE AND MAXIMUM ENTROPY METHODS IN SCIENCE AND ENGINEERING. AIP, 2002. http://dx.doi.org/10.1063/1.1477035.

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Makar, Karen W., E. M. Poole, L. Xiao, C. F. Rimorin, R. L. Galbraith, M. L. Slattery, D. Duggan i in. "Abstract 5710: COX-1 and COX-2 polymorphisms, NSAID use, and the risk of colorectal neoplasia". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5710.

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Moço, Amanda Cristina, Prof Dr Renato Massaharu Hassunuma, Marlon Marcio Ferreira Urata i Prof A. Dr A. Patrícia Carvalho Garcia. "Uma visão pela Bioinformática da inibição da ciclo-oxigenase-2 pelo anti- inflamatório indometacina". W II Congresso Brasileiro de Bioquímica Humana On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbraqui/14.

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Introdução: Os anti-inflamatórios não esteroidais (AINEs) estão entre os fármacos mais utilizados na prática médica. Destacam-se pela grande variedade de indicações terapêuticas. A indometacina (IMN) é um AINE utilizado em casos de osteoartrite, artrite reumatoide moderada ou severa, tendinites, espondilite anquilosante, antipirético e cefaleia responsiva à indometacina. O efeito anti-inflamatório da IMN resulta da inibição da ciclo-oxigenase-2 (COX-2), uma enzima que participa da produção de mediadores inflamatórios como prostaglandinas e tromboxanos. Objetivos: O objetivo principal da presente pesquisa foi o desenvolvimento de scripts para o software RasMol 2.7.4.2, no intuito de produzir imagens que ilustrem a interação entre a IMN e a COX-2. Material e métodos: Foi realizado o levantamento de arquivos PDB sobre a IMN e a COX-2, obtidos no site Protein Data Bank. Foram selecionados arquivos PDB de acordo com critérios como data de upload do arquivo, nível de resolução da estrutura cristalizada, método experimental utilizado, entre outros. A partir dos arquivos PDB selecionados, foram desenvolvidos vários scripts para o software RasMol. Resultados: As imagens obtidas no programa computacional RasMol mostraram que a IMN se liga a uma região relativamente profunda de um canal hidrofóbico da COX-2. A ligação da IMN e a COX-2 ocorre por meio de uma interação entre um átomo de cloro da IMN com o resíduo de aminoácido leucina 384 da COX-2. A estabilização da ligação entre estas substâncias ocorre também por meio de interações hidrofóbicas da região benzoíla da IMN com a leucina 384, fenilalanina 381, tirosina 385 e triptofano 387, bem como do átomo de oxigênio do grupo benzoila da IMN com a hidroxila da cadeia lateral da serina 530 e a cadeia lateral da valina 349 da COX-2. Conclusão: As imagens produzidas a partir dos scripts mostraram que a ligação da IMN com a COX-2 ocorre por meio de interações com resíduos de aminoácidos da COX-2 de modo diferente que ocorre quando comparado com outros inibidores. O estudo bioquímico estrutural dos diferentes inibidores da COX-2, como a IMN, pode ser importante para o desenvolvimento de novos anti-inflamatórios sintéticos não seletivos.
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Yu, Shipeng, Glenn Fung, Romer Rosales, Sriram Krishnan, R. Bharat Rao, Cary Dehing-Oberije i Philippe Lambin. "Privacy-preserving cox regression for survival analysis". W the 14th ACM SIGKDD international conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1401890.1402013.

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Al-Khalil, Kamel, Laszlo Salamon i Gary Tenison. "Development of the Cox Icing Research Facility". W 36th AIAA Aerospace Sciences Meeting and Exhibit. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1998. http://dx.doi.org/10.2514/6.1998-97.

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Safholm, J., K. Stark, L. Cardell, S. Dahlen i M. Adner. "EP1Receptor Mediates the Intrinsic Tone in Guinea-Pig Trachea Via Secretion of PGE2Generated from COX-1 and COX-2." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6323.

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Zhao, Z., i D. Wei. "MAMR frequency optimization on [CoX/Pt]4 media". W 2017 IEEE International Magnetics Conference (INTERMAG). IEEE, 2017. http://dx.doi.org/10.1109/intmag.2017.8007582.

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Jeong, Youngmin, Dung Phuong Trinh i Hyundong Shin. "V2V communication in a Cox field of vehicles". W 2014 International Conference on Connected Vehicles and Expo (ICCVE). IEEE, 2014. http://dx.doi.org/10.1109/iccve.2014.7297686.

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Sari, D. J., D. Lestari i S. Devila. "Pricing life insurance premiums using Cox regression model". W PROCEEDINGS OF THE 4TH INTERNATIONAL SYMPOSIUM ON CURRENT PROGRESS IN MATHEMATICS AND SCIENCES (ISCPMS2018). AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5132461.

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Raporty organizacyjne na temat "Cox"

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Levine, Alice C. COX-2 and Prostate Cancer Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, marzec 2002. http://dx.doi.org/10.21236/ada405593.

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Levine, Alice C. COX-2 and Prostate Cancer Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, marzec 2003. http://dx.doi.org/10.21236/ada420162.

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Reddy, E. P. Novel COX-2 Inhibitor for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2005. http://dx.doi.org/10.21236/ada444637.

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Reddy, E. P. Novel Cox-2 Inhibitor for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2004. http://dx.doi.org/10.21236/ada431390.

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Reddy, E. P. Novel COX-2 Inhibitor for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2003. http://dx.doi.org/10.21236/ada420352.

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Martín Sanz, Paloma. Papel dual de Cox-2 en la fisiopatología hepática. Sociedad Española de Bioquímica y Biología Molecular, kwiecień 2016. http://dx.doi.org/10.18567/sebbmdiv_anc.2016.04.1.

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Burr, Deborah. A Study of Bootstrap Confidence Intervals in a Cox Model. Fort Belvoir, VA: Defense Technical Information Center, lipiec 1992. http://dx.doi.org/10.21236/ada254598.

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Karr, Alan F. State Estimation for Cox Processes with Unknown Law: Parametric Models. Fort Belvoir, VA: Defense Technical Information Center, listopad 1985. http://dx.doi.org/10.21236/ada166179.

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Di Capua, M. S. Cox report and the US-China arms control technical exchange program. Office of Scientific and Technical Information (OSTI), wrzesień 1999. http://dx.doi.org/10.2172/15006866.

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Chintadunta, Pradeep, Renna Jiang i Ginger Jin. Information, Learning, and Drug Diffusion: the Case of Cox-2 Inhibitors. Cambridge, MA: National Bureau of Economic Research, sierpień 2008. http://dx.doi.org/10.3386/w14252.

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