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Dissertations / Theses on the topic 'Arachidonic acid'

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Published: 4 June 2021
Last updated: 8 June 2024

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1

Mantri, Padmaja. "Arachidonic acid aci-Reductone strategies : asymmetric synthesis of 2-hydroxytetronic acid antimetabolities /." The Ohio State University, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487848078452092.

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2

Berry, Elicia Bee Ean. "Intracellular signalling by arachidonic acid metabolites." Thesis, University of Auckland, 2006. http://hdl.handle.net/2292/3111.

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In intrauterine tissues, pro-inflammatory cytokines and prostaglandins (PGs) have been identified as key mediators in the maintenance of pregnancy and parturition. The rise in PGD2 detected in the amniotic fluid before labour prompted the research presented in this thesis which describes the effects of 15-deoxy Δ12,14 -prostaglandin J2 (15d-PGJ2), a non-enzymatic metabolite of PGD2, on amnion-derived WISH and JEG3 choriocarcinoma cells as models of the amnion and chorion trophoblasts, respectively.15d-PGJ2 induced apoptosis in both cell lines in a concentration-dependent fashion (2.5-10 µM). Apoptosis was characterised by condensation of chromatin (visualised after Hoechst 33342 staining), appearance of nucleosomal DNA fragmentation upon electrophoresis and flow cytometry analysis, and activation of caspase-3. Apoptotic cell death was inhibited in the presence of serum (0.5% w/v) and albumin, not serumderived growth factors (insulin growth factor (IGF)-1, IGF-2 or epidermal growth factor (EGF), was determined as the key survival factor. Since 15d-PGJ2 is reported to activate peroxisome proliferator activated receptor (PPAR)-γ, the activities of PPARs were assessed using JEG3 cells transfected with a PPAR-response element reporter construct (pTK-PPREx3-luc). The PPAR-γ-specific ligand, rosiglitazone, induced PPRE mediated activity in a concentration-dependent manner, while the PPAR-γ-specific irreversible inhibitor, GW9662, fully inhibited this induction. However, GW9662 only partially inhibited 15d-PGJ2-induced luciferase activity, suggesting that 15d-PGJ2 may also activate either of the other isoforms. The expressions of PPAR-α and -δ were identified in amnion, choriodecidua and placental membranes and PPAR-δ was significantly increased all tissues with labour. PPAR-α expression was reduced in chorio-decidua, but was significantly higher in placenta with labour. The changes observed with labour suggest that regulation of PPAR expression and function may have a role in the mechanisms that maintain pregnancy or initiate labour. The anti-inflammatory effects of 15d-PGJ2 were also investigated by measuring interleukin (IL)-1β-stimulated prostaglandin and cytokine productions by WISH cells after treatment with 15d-PGJ2 for 3 hours. 15d-PGJ2 exerted differential effects that were dependent upon its concentration. At low nanomolar physiologic concentrations (1-10 nM), 15d-PGJ2 inhibited IL-1β-stimulated PGE2, but not cytokine (IL-6/IL-8) production or cyclooxygenase (COX)-2 expression. This effect was attenuated by GW9662, by transfection with dominant negative PPAR constructs, and was reproduced by rosiglitazone. At micromolar (1-10 µM) concentrations, 15d-PGJ2 inhibited IL-1β-stimulated COX-2, PGE2 and cytokine productions and these effects were not blocked by GW9662 or mimicked by rosiglitazone. GW501516 (PPAR-δ agonist) also inhibited IL-1β-stimulated PGE2 production, but only at high concentrations (1 µM). IL-1β-induced NF-kB DNA binding activity was significantly inhibited by 15d-PGJ2 (10 µM) and GW501516 (1 µM), but increased by rosiglitazone (10 µM). In conclusion, this is the first report of an effect of 15d-PGJ2 at low nanomolar physiologic concentrations and 15d-PGJ2 mediates its actions through PPAR-γ (<0.1 µM) and PPAR-γ-independent(1-10 µM) pathways, the latter through inhibition of NF-kB and/or activation of PPAR-δ. Further studies on the effect of physiologic concentrations of 15d-PGJ2 on primary gestational tissues will provide understanding on the role(s) 15d-PGJ2 plays in fetal membrane remodelling and its involvement in the inflammatory processes associated with labour and parturition.
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3

Hewertson, S. J. "Arachidonic acid metabolism by liver and hepatoma." Thesis, Brunel University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379706.

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4

樊曉明 and Xiaoming Fan. "Arachidonic acid metabolism in apoptosis of gastric cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31241633.

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5

Fan, Xiaoming. "Arachidonic acid metabolism in apoptosis of gastric cancer." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22805448.

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6

Tsai, I.-Jung. "Perturbations of arachidonic acid metabolism in the metabolic syndrome." University of Western Australia. School of Medicine and Pharmacology, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0065.

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[Truncated abstract] Arachidonic acid is oxidised in vivo by non-enzymatic (free radical) or enzymatic pathways (cyclooxygenase, lipoxygenase, and cytochrome P450) to form a range of biologically active eicosanoids. Specifically, arachidonic acid is metabolised by cytochrome P450 -hydroxylase to produce vasoactive 20-hydroxyeicosatetraenoic acid (20-HETE), and by 5-lipoxygenase to produce proinflammatory leukotriene B4 (LTB4), which can further be metabolised by -hydroxylase to from 20-OH-LTB4 and 20-COOH-LTB4. F2-Isoprostanes (F2-IsoPs) are produced through free radical attack on arachidonic acid and have been recognised as the most reliable markers of lipid peroxidation in vivo. The metabolic syndrome (MetS) is characterised by abdominal obesity, hypertension, insulin resistance, glucose intolerance, and dyslipidemia. It is associated with low-grade inflammation and oxidative stress and an increased risk of developing cardiovascular diseases. Dietary weight loss is strongly recommended for the management of the MetS and can potentially minimise the risk of cardiovascular diseases and diabetes in individuals with the MetS. Little is known regarding the role of these arachidonic acid metabolites in the MetS and the effect of weight loss on their metabolism. Chapter three comprised of three in vitro studies aimed to examine 20-HETE synthesis in human blood cells. 20-HETE acts as a second messenger for vasoconstrictor actions of angiotensin II (Ang II) and endothelin-1 (ET-1) in renal and mesenteric beds. Human neutrophils and platelets are integral to the inflammatory process. ... Production of LTB4 and 20-OH-LTB4 was significantly lower compared with controls (P<0.005) and remained so after adjustment for neutrophil count (P<0.05).The weight loss intervention resulted in a 4.6kg reduction in body weight and a 6.6cm decrease in waist circumference and a significant increase in LTB4 and 20-OH- LTB4 in the weight loss group. Chapter Five continued to investigate the role of other arachidonic acid metabolites, 20-HETE and F2-IsoPs in the MetS and the effect of weight loss. In the case-control study (Human study 1), plasma and urinary 20-HETE and F2-IsoPs were significantly elevated in the MetS group, but no significant difference was found in stimulated-neutrophil 20-HETE. A significant gender x group interaction was observed in that women with the MetS had higher urinary 20-HETE and F2-IsoPs compared to controls (P<0.0001). In a randomised controlled trial (Human study 2), relative to the weight- maintenance group, a 4.6 kg loss in weight resulted in a 2 mmHg fall in blood pressure but did not alter the production of 20-HETE or F2-IsoPs. No significant differences were shown in 20-HETE released from stimulated-neutrophils before and after weight loss. 20-HETE and oxidative stress may be important mediators of cardiovascular disease risk in the MetS. Although a 4% reduction in body weight reduced BP, there were no changes in plasma or urinary 20-HETE or F2-IsoPs. In summary, in vitro studies show that human neutrophils and platelets can produce 20-HETE in response to Ang II and ET-1, and human studies demonstrate that the presence of MetS has a significant impact on arachidonic acid metabolism and effective weight loss can restore leukocyte synthesis of LTB4.
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7

Mollapour, Elahe. "The role of arachidonic acid mobilisation in myeloid cells." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313822.

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8

Saunders, Royal Duane. "Arachidonic acid and lipid metabolism following spinal cord injury /." The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487260859496213.

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9

CHIESA, FRANCESCO. "SYNTHETICAL STUDIES ON ARACHIDONIC ACID METABOLITES FOR DIAGNOSTIC PURPOSES." Doctoral thesis, Università degli studi di Pavia, 2017. http://hdl.handle.net/11571/1203279.

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Prostaglandins (PGs) are the principal metabolites of arachidonic acid. The basic prostaglandin skeleton is that of a cyclized C20 fatty acid containing a cyclopentane ring, a C7 side-chain with the carboxyl function (α-chain), and a C8 side-chain with the methyl terminus (ω-chain). They are now known to occur widely in animal tissues, but only in tiny amounts, and they have been found to exert a wide variety of pharmacological effects on humans and animals. The quantification of PGs in biological fluids is often affected by artifacts or ex vivo generation of these molecules during the sampling. The measurement of free eicosanoids and their metabolites in urine is a non-invasive and representative method for the determination of their systemic production. For these reasons the synthesis of prostaglandins derivatives is important to obtain useful standards for diagnostic purposes. With this study we propose a new synthesis of the PGE2-urinary metabolite and the synthetical study on the probable urinary metabolite of the 15d-PGJ2.Both synthetical approaches use the TBS-Corey Aldehyde as principal building block that permit easy and flexible three component stnthesis.
Prostaglandins (PGs) are the principal metabolites of arachidonic acid. The basic prostaglandin skeleton is that of a cyclized C20 fatty acid containing a cyclopentane ring, a C7 side-chain with the carboxyl function (α-chain), and a C8 side-chain with the methyl terminus (ω-chain). They are now known to occur widely in animal tissues, but only in tiny amounts, and they have been found to exert a wide variety of pharmacological effects on humans and animals. The quantification of PGs in biological fluids is often affected by artifacts or ex vivo generation of these molecules during the sampling. The measurement of free eicosanoids and their metabolites in urine is a non-invasive and representative method for the determination of their systemic production. For these reasons the synthesis of prostaglandins derivatives is important to obtain useful standards for diagnostic purposes. With this study we propose a new synthesis of the PGE2-urinary metabolite and the synthetical study on the probable urinary metabolite of the 15d-PGJ2.Both synthetical approaches use the TBS-Corey Aldehyde as principal building block that permit easy and flexible three component stnthesis.
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10

溫志友 and Zhiyou Wen. "A high yield and productivity strategy for eicosapentaenoic acid production by the diatom Nitzschia laevis in heterotrophic culture." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31242418.

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11

Harding, Pamela. "Glomerular prostanoid production in rats : the influence of angiotensin converting enzyme inhibition." Thesis, Keele University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385190.

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12

Wen, Zhiyou. "A high yield and productivity strategy for eicosapentaenoic acid production by the diatom Nitzschia laevis in heterotrophic culture." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23242097.

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13

Roberts, Tomos Huw. "Synthetic approaches towards novel cyclooxygenase and lipoxygenase inhibitors." Thesis, Bangor University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265240.

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14

Schultz, Jeffrey Allen. "Approaches to the synthesis of hydroperoxyeicosatetraenoic acids (HPETES) : 1. directed oxygenations, 2. additions to peroxycarbenium ions." [Lincoln, Neb. : University of Nebraska-Lincoln], 1999. http://international.unl.edu/Private/1999/schultzab.pdf.

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15

Rose, Matthew P. "Arachidonic acid metabolism by human fetal membranes in tissue culture." Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37838.

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16

Mootoo, Judy E. (Judy Elizabeth). "Lipoxygenase metabolites of arachidonic acid in the porcine ovulatory process." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22779.

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It is widely accepted that prostaglandins (PGs), produced via the cyclooxygenase pathway from arachidonic acid, are essential to the ovulatory process in the pig. In support of this, ovulation is preceded by an increase in follicular fluid (FF) PG concentration, indomethacin (INDO) suppresses both the PG increase and ovulation, and ovulation can be restored by administration of exogenous PGs (Downey and Ainsworth, 1980; Prostaglandins 19: 17-22). Recent studies in the rat have shown that ovulation is also preceded by a rise in ovarian concentrations of 15-hydroxyeicosatetraenoic acid (15-HETE), a product of the lipoxygenase pathway (Tanaka et al., 1989; Endocrinology 15: 1373-1377) and inhibition of this pathway suppresses ovulation (Reich et al., 1983; Prostaglandins 26: 1011-1020). Furthermore, INDO, a cyclooxygenase inhibitor, inhibits 15-lipoxygenase as well as PG synthesis (Tanaka et al., 1989 Endocrinology 15: 1373-1377). The PMSG/hCG prepuberal gilt model was used to investigate the involvement of 15-HETE in the procine ovulatory process, and the effect of INDO on the 15-lipoxygenase pathway. Follicular fluid concentrations of 15-HETE were elevated 40 h post hCG (p $<$ 0.01). The effects of INDO and nordihydroguaiaretic acid (NDGA), an inhibitor of lipoxygenase activity, on ovulation rate, FF 15-HETE and FF PGF$ rm sb{2a}$ were investigated by intraovarian administration of INDO or NDGA. INDO inhibited ovulation rate (p $<$ 0.01) and PGF$ rm sb{2a}$ (p $<$ 0.01) as well as 15-HETE (p $<$ 0.01). NDGA also suppressed ovulation rate (p $<$ 0.01) but did not inhibit 15-HETE or PGF$ rm sb{2a}$ production. In in vitro experiments, 15-HETE production by both granulosa cell (GC) and theca interna cell (TIC) cultures 40 h post hCG was greater (p $<$ 0.01) than at 0 h post hCG. INDO inhibited 15-HETE production in 40 h post hCG TIC cultures (p $<$ 0.01) but not GC cultures, while NDGA inhibited 15-HETE production by both cell types (p $<$ 0.01). These results sugges
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17

Boughton-Smith, N. K. "The role of arachidonic acid metabolites in inflammatory bowel disease." Thesis, King's College London (University of London), 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372374.

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18

Malipa, Ana Chimuemue Antonio. "Uptake of arachidonic acid and glucose into isolated human adipocytes." Diss., University of Pretoria, 2007. http://hdl.handle.net/2263/23930.

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Both plasma glucose concentration and glucose uptake are deranged in insulin resistance. A high free fatty acid plasma level is a potential cause of insulin resistance, and therefore of type 2 diabetes mellitus animals and humans. The mechanism behind this is still unclear. The objectives of the present study were: (i) to research the effect of arachidonic acid (AA) as fatty acid representative, on glucose uptake into human isolated adipocytes, (ii) to investigate the uptake of AA into adipocyte membranes and nuclei, as a step to identify the mechanism whereby AA affects glucose uptake, and (iii) to verify the influence of insulin on AA uptake in adipocytes. The first objective was achieved by exposing adipocytes to AA and measuring the effect on deoxyglucose uptakt. To achieve the second objective, adipocytes were exposed to 14C-AA; radioactive uptake in membranes and nuclei was determined. The AA uptake into membranes was also determinate by membranes fatty acid profile using gas chromatography; the results of the two methods were compared. Finally, the third objective was achieved by exposing adipocytes to different concentrations of insulin and testing the effect by measuring arachidonic acid uptake by the entire cell. The results of this study shown that, acute (30 min) exposure of AA significantly stimulates glucose uptake by adipocytes (4.56 ± 0.6 nmole glucose /mg protein /min) compared to the control (3.12 ± 0.25 nmole glucose /mg protein /min). Secondly, 14C-AA was significantly taken up by the membranes between 20 and 30 minutes of exposure. The uptake into membranes was increased by 49.57 ± 29% and 123 ± 73% compared to the control 100% (1.77 ± 0.06 nmole AA /mg protein) respectively for 20 and 30 min exposure). AA significantly rose in the nuclei after 30 minutes (147 ± 19% increase) compared to the control 100% (2.25 ± 0.10 nmole AA /mg protein). The determination of AA uptake by gas chromatography analysis of the membrane fatty acid profile showed that the content of AA increased after 30 min exposure (0.57% AA of total membrane fatty acids) compared to the 10 min exposure (0.29% AA of total membrane fatty acid). Insulin was shown to stimulate 10 and 30 min AA uptake by adipocytes from a non-obese subject. The increases of AA uptake measured for 30 minutes were 20 ±8%, 21 ± 25% and 31 ± 4% compared to the control (0.58nmole AA / mg protein / min) respectively for the actions of 10nM, 20nM and 40 nM insulin. A similar tendency was observed when the AA uptake was measured for 10 min (81 ± 31% and 208 ± 36% respectively for the action of 10nM and 40nM insulin compared to the control 100% (0.06nmole AA/mg protein/min). In contrast to this finding, insulin depressed AA uptake by adipocytes from an obese subject (depression of 15 ± 5%, 14 ± 8% and 21 ± 5% respectively for 10nM, 20nM and 40nM insulin, compared to the control 100% (0.74 nmole AA/mg protein/min). In both situations the effect of insulin seemed dose dependent. The study demonstrated that AA acid positively modulates glucose uptake into adipocytes exposed for short periods (< 30 min). This was attributed to the probable this FA in the cell membrane, rather than its eventual effect on the DNA. The best method to measure membranes AA over short period of exposure when small amounts of adipocytes (2- 6 ml) are used was by radioactive means. It also suggested that insulin effect’s on AA acid uptake into adipocytes was dose dependent. This varies with the body mass index (BMI) of the patient, probably as a result of their cell’s insulin resistant state.
Dissertation (MSc (Veterinary Science))--University of Pretoria, 2007.
Anatomy and Physiology
MSc
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19

Malipa, Ana Chimuémue António. "Uptake of arachidonic acid and glucose into isolated human adipocytes." Pretoria : [s.n.], 2007. http://upetd.up.ac.za/thesis/available/etd-04112008-163537/.

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20

Müller, Urs. "New assay to measure oxygenation of arachidonic acid in platelets /." [S.l.] : [s.n.], 1991. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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21

Talukdar, Indrani. "Signaling pathways involved in regulation of glucose-6-phosphate dehydrogenase (G6PD) by arachidonic acid." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4673.

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Thesis (Ph. D.)--West Virginia University, 2006.
Title from document title page. Document formatted into pages; contains viii, 123 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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22

招志明 and Chi-ming Lawrence Chiu. "Possible mechanisms of arachidonic and eicosapentaenoic acids on humanleukemic cell proliferation and apoptosis by flow cytometric analysis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31236741.

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23

Chiu, Chi-ming Lawrence. "Possible mechanisms of arachidonic and eicosapentaenoic acids on human leukemic cell proliferation and apoptosis by flow cytometric analysis /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19737907.

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24

Williams, John Huw. "Presynaptic mechanisms in the maintenance of long-term potentiation : an in-vitro investigation in the hippocampus." Thesis, University College London (University of London), 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293999.

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25

Harder, Hubert Werner. "Metabolism of arachidonic and adrenic acids in molecular species of gycerophospholipids in mouse brain /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu14872651431456.

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26

Secreto, Frank. "The regulation of arachidonic acid metabolism in human osteoblast-like cells." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2970.

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Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains vi, 123 p. : ill. Includes abstract. Includes bibliographical references (p. 110-123).
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27

Tran, Khai T. "Vitamin E and arachidonic acid metabolism in cultured human endothelial cells." Thesis, University of Ottawa (Canada), 1990. http://hdl.handle.net/10393/5839.

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A novel approach to study the metabolism of nutrients in human cells was developed. The incorporation and depletion of 2R,4$\sp\prime$R,8$\sp\prime$R-$\alpha$-tocopherol (RRR-$\alpha$-T), a natural form of vitamin E, and its subsequent effect on the metabolism of arachidonic acid were conducted on human umbilical vein endothelial cells (HUVECs) in culture. HUVECs incorporated physiological and pharmacological concentrations of RRR-$\alpha$-T in a time- and dose-dependent manner. Incorporated tocopherol was found mainly associated with membrane fractions of the cell. This stimulatory activity of tocopherol has an absolute structural requirement for both free hydroxyl moiety and the hydrophobic phytyl side chain, although the position and the presence of the methyl groups attached to the aromatic moiety are not required for its activity. Direct analysis of enzymes involved in phospholipid metabolism indicated that tocopherol-enrichment caused an increase in phospholipase A$\sb2$ activity without affecting the activities of lysophospholipase or acylCoA-acyltransferase. Hydrogen peroxide when combined with $\alpha$-tocopherol synergistically stimulated basal release of PGI$\sb2$ from endothelial cells. $\alpha$-tocopherol potentiates PGI$\sb2$ synthesis when challenged with exogenous arachidonic acid. (Abstract shortened by UMI.)
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28

Feltenmark, Stina. "Studies on arachidonic acid metabolism in normal and malignant hematopoietic cells." Stockholm : Division of Physiological Chemistry II, Karolinska Institutet, 2010. http://diss.kib.ki.se/2010/978-91-7409-745-0/.

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29

Sayre, Brian L. "Arachidonic acid metabolism by early ovine embryos and the role of prostaglandins in one aspect of embryonic development." Thesis, This resource online, 1991. http://scholar.lib.vt.edu/theses/available/etd-10102009-020219/.

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30

Brown, Stacy D., Martha Borketey, and Sharon Campbell. "LC-MS-MS Determination of Arachidonic Acid and Linoleic Acid Product Profiles in Colon Cancer Cells." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/5276.

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31

Usman, Rukhsana. "Platelet activity and arachidonic acid metabolism: modulation by factors in plasma and cerebrospinal fluidand by diet." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1994. http://hub.hku.hk/bib/B31233934.

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32

Reid, Morag. "Group I mGlu receptors : desensitization properties and modulation of cerebrocortical glutamate release." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311428.

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Usman, Rukhsana. "Platelet activity and arachidonic acid metabolism : modulation by factors in plasma and cerebrospinal fluid and by diet /." [Hong Kong] : University of Hong Kong, 1994. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13787263.

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34

Kennedy, Christopher R. J. "Signalling pathways of bradykinin-mediated arachidonic acid release in MDCK-D1 cells." Thesis, University of Ottawa (Canada), 1997. http://hdl.handle.net/10393/4074.

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An investigation was undertaken to elucidate the signal transduction pathways involved in bradykinin (BK)-mediated release of arachidonic acid (AA) from the D1 clone of Madin-Darby canine kidney cells (MDCK-D1) which display distal tubule- and cortical collecting duct principal cell-like characteristics. Prostaglandins (PG), generated subsequent to BK stimulation, are known to modulate arginine-vasopressin (AVP)-stimulated water flow across this portion of the nephron. The enzyme immediately responsible for AA release was determined to be the 85 kDa cytosolic phospholipase A$\sb2$ (cPLA$\sb2),$ since Western blots revealed the presence of this enzyme and its specific inhibition by an arachidonate analogue completely blunted BK-stimulated AA release. Additionally, in vitro PLA$\sb2$ activity could be significantly reduced by preincubating cell lysates with an antibody to this enzyme. Lastly, this in vitro activity met all the requirements specific to cPLA$\sb2,$ including activity at micromolar Ca$\sp{2+}$ concentrations and dithiotreitol (DTT)-insensitivity. The findings herein suggest the signalling route taken for BK-induced AA release involves phosphatidyicholine-specific phospholipase C (PC-PLC) as well as phospholipase D (PLD). Accordingly, production of sn-1,2-diacylglycerol (DAG) and to a lesser extent, phosphatidic acid (PA), both contribute to this release of AA by enhancing PLA$\sb2$ activity within the cellular membranes, whereas the activation of phosphatidylinositol-specific phopholipase C (PI-PLC) and subsequent inositol trisphosphate (InsP$\sb3$) production does not. While reports indicate the activation of protein kinase C (PKC) is required for epinephrine-mediated AA release in this cell line, inhibition of PKC failed to abrogate BK-stimulated AA release. On the other hand, down regulation of PKC levels via long-term incubation with phorbol ester (PMA) reduced both BK- and calcium ionophore (A23187)-induced AA release. However, both in vitro cPLA$\sb2$ activity and its phosphorylation, but not its expression, were significantly reduced subsequent to long-term PMA treatment, thereby demonstrating that this strategy falsely implicates immediate activation of PKC as being required for BK-mediated AA release. Extracellular calcium (Ca$\sp{2+})$ was also needed for AA release as blockade of receptor-operated Ca$\sp{2+}$ channels significantly decreased BK-induced AA release. In addition, a negative regulatory pathway in MDCK cells was demonstrated which diminishes BK-mediated AA release. Agents which cause elevations in adenosine-3$\sp\prime,5\sp\prime$-cyclic monophosphate (cAMP) levels, such as AVP or forskolin (FSK) and 3-isobutyl-1-methylxanthine (IBMX), were found capable of significantly reducing BK-induced AA release and in vitro PLA$\sb2$ activity. This method of inhibition could represent a physiological mechanism of negative feedback promoted by agents which increase cAMP levels within the cells of the distal tubule and collecting duct. Possible targets for inhibition are suggested in light of results obtained in the present thesis and reported by others.
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35

Kennedy, Chris R. J. "Signalling pathways of bradykinin-mediated arachidonic acid release in MDCK-D1 cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21003.pdf.

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McCallum, Gordon P. "Modulation of cytochrome P450-dependent arachidonic acid metabolism by polycyclic aromatic hydrocarbons." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0014/NQ42545.pdf.

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37

Roberts, Michael D. Kreider Richard B. "Effects of arachidonic acid supplementation on training adaptations in resistance-trained males." Waco, Tex. : Baylor University, 2006. http://hdl.handle.net/2104/4890.

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38

Phythian, Sara. "The synthesis of aromatic analogues of leukotriene B←4 and arachidonic acid." Thesis, University of East Anglia, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327931.

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39

Habbel, Jan-Piet [Verfasser]. "Docosahexaenoic acid suppresses arachidonic acid-induced proliferation of LS 174T human colon carcinoma cells / Jan-Piet Habbel." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/1030380562/34.

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40

Mann, Neil James, and mikewood@deakin edu au. "The effect of dietary arachidonic acid and n-3 polyunsaturated fatty acids on the production of eicosanoids." Deakin University. School of Nutrition and Public Health, 1995. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20051125.105437.

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The major polyunsaturated fatty acid (PUFA) in the western diet is linoleic acid (LA), which is considered to be the major source of tissue arachidonic acid (AA), the principal precursor for the vaso-active eicosanoids via the cyclooxygenase enzymatic pathway. However, dietary AA may contribute significantly to tissue levels of AA in humans, leading to an increase in the production of eicosanoids, particularly the platelet aggregating, vasoconstricting, thromboxane (TXA2), hence increasing thrombosis risk. The aims of this study were to determine the extent to which dietary AA contributed to prostacyclin (PGI2) and TXA2 production in vivo and whether dietary long chain (LC) n-3 PUFA have a modulating influence on the metabolism of AA to these vaso-active eicosanoids. A gas chromatography -mass spectrometry (GCMS) method for urinary PGI2-M determination and a tandem GCMS/MS method for urinary TXA2-M determination were perfected for use within our laboratory (with the assistance of Dr Howard Knapp, University of Iowa and Professor Reinhard Lorenz, Ludwig Maximilian's University, Munich, respectively). An initial animal study compared the in vitro production of PGI2 by aorta segments with the whole body in vivo production of PGI2 in rats fed ethyl arachidonate or the ethyl ester of eicosapentaenoic acid (EPA), at levels many times higher than encountered in human diets. During AA feeding both measures of PGI2 increased, although in vitro TXA2 production was not affected. EPA feeding lowered in vitro TXA2 and in vivo PGI2. Prior to determining the effects of AA and LC n-3 PUFA in humans, a study was carried out to determine the AA and LC n-3 PUFA content of foods and from these, an estimate of the mean daily intake of AA and other LC PUFA. Eggs, organ meats and paté were found to be the richest sources of AA. Of the meat and fish analysed, white meat was found to be relatively rich in AA but poor in LC n-3 PUFA. Lean red meat, particularly kangaroo had similar LC n-3 PUFA and AA content. Fish, although rich in AA, had extremely high levels of LC n-3 PUFA. The calculated mean daily intakes of AA in Australian adults was 130mg (males) and 96mg (females). For total LC n-3 PUFA intake, the mean daily values were 247mg (males) and 197mg (females). Two human pilot studies involving dietary intervention trials examined the effects of dietary AA and AA plus long chain n-3 PUFA on thrombosis risk, gauged by the change in the ratio of PGI2 / TXA2 as well as alterations to other recognised risk factors, such as lipoprotein lipids and platelet aggregation. The desired dietary amounts of AA and LC n-3 PUFA were achieved in the first study by combining food items with known levels of each fatty acid. In the second study, where a diet with approximately equal quantities of AA and LC n-3 PUFA was being examined, kangaroo meat was consumed, following a low-fat vegetarian diet used as a baseline. Diets rich in AA alone (~500mg/day) increased plasma phospholipid (PL) AA levels, PGIi and TXA2 production. When foods containing equal quantities of AA and EPA (∼500mg/day of each) were fed to subjects PGI2 increased, with no change in TXAs production. Low fat vegetarian diets lowered PGI2 production, the level of which was reestablished by an AA rich diet (∼300mg AA/day + ∼260mg/day LC n-3 PUFA) of kangaroo meat. However, TXA2 production was not altered. A final, larger human dietary intervention trial then examined the effects of diets relatively rich in AA alone, AA plus LC n-3 PUFA and LC n-3 PUFA, on the ratio of PGI2/TXA2- The dietary sources of these fatty acids were white meat, red meat and fish, respectively. Each contained a mean level of AA of ∼140mg/day, with varying LC n-3 PUFA levels (59, 161 and 3380mg/day, respectively). Neither meat diet altered PGI2 or TXA2 production significantly, despite increasing serum PL AA levels. The fish diet resulted in a decrease in the serum and platelet PL AA/EPA ratio and TXA2 production, thus increasing the PGI2 / TXA2 ratio. These results would indicate that stores of AA in the body are sufficiently high to have effectively saturated the cyclooxygenase pathway for production of both PGI2 and TXA2, thus making any small change in the plasma level of AA due to 'normal' dietary levels, inconsequential. However, as seen in the rat study and the two pilot studies higher dietary levels of AA can increase both PGI2 and TXA2 production. Increases in platelet levels of EPA and DHA were associated with a decrease in TXA2 production, or the maintenance of a constant TXA2 level, while AA tissue levels and PGI2 production increased. This suggests a possible inhibitory effect of LC n-3 PUFA on the metabolism of AA to TXA2, particularly in platelets. From these short term studies, conducted over 2-3 week periods, it can be concluded that diets rich in lean meats can raise plasma AA levels but do not affect TXA2 or PGI2 production, hence are not pro-thrombotic. Diets rich in long chain n-3 PUFA from fish, raise plasma EPA and DHA levels, lower TXA2 production and are anti-thrombotic. Diets which combine equal quantities of AA and LC n-3 PUFA appear to increase PGI2 production while keeping TXA2 production constant. In order for these LC PUFA to have a significant effect on eicosanoid production the dietary intake of these fatty acids through foods such as red meat or white meat would have to be higher than average current Australian consumption levels.
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41

St-Pierre, Sylvie. "The impact of arachidonic acid supplements and dietary fat on blood glucose control /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18552.pdf.

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42

Zosmer, Ariel. "Control of progesterone production during early pregnancy : the role of arachidonic acid metabolites." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286759.

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43

Leng, Xinyan. "Roles of proteasome, arachidonic acid, and oxytocin in bovine myoblast proliferation and differentiation." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/82707.

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The overall objective of this dissertation project was to identify factors and mechanisms that control bovine myoblast proliferation, differentiation, and fusion. Three studies were conducted during this project. The objective of the first study was to determine the effect of oxytocin (OXT) on myoblast proliferation, differentiation and fusion. Treating primary bovine myoblasts in culture with 10 nM and 100 nM OXT for 24 h increased their proliferation rate by 7% (P < 0.05) and 10% (P < 0.05), respectively. Treating bovine myoblasts with either concentration of OXT for 48 h had no effect on their differentiation and fusion, as indicated by no changes in mRNA expression of selected myoblast differentiation markers and fusion index. The objective of the second study was to determine the effects of arachidonic acid (AA) and its major metabolites prostaglandin E2 (PGE2), PGF2a, and PGI2 on myoblast proliferation, differentiation and fusion. Treating myoblasts with 10 μM AA, 1 μM PGE2, 1 μM PGF2α, and 1 μM PGI2 for 24 h each increased the number of proliferating cells by 13%, 24%, 16%, and 16%, respectively, compared to the control (P < 0.05). At the same concentrations, AA, PGE2, and PGF2a stimulated myoblast differentiation and PGE2 improved myoblast fusion (P < 0.05). Treating myoblasts with AA and the cyclooxygenase (COX)-1 and COX-2 inhibitor indomethacin or the COX-2-specific inhibitor NS-398 reversed the stimulatory effect of AA on myoblast proliferation (P < 0.05). The objective of the third study was to determine the role of the proteasome in bovine myoblast differentiation and fusion. It was found that the proteasome activity increased (P < 0.05) during myoblast differentiation and fusion. Adding 5 μM lactacystin, a specific inhibitor of the proteasome, to the differentiation medium nearly completely blocked myoblast differentiation and fusion. Inhibitor of DNA-binding 1 (ID1) is known to inhibit myoblast differentiation and to be degraded by the proteasome in some cells. Both ID1 protein and mRNA expression were found to decrease during myoblast differentiation and fusion, and the decrease in ID1 protein but not ID1 mRNA was reversed (P < 0.05) by treating the cells with lactacystin. In summary, this project reveals that OXT and AA are stimulators of bovine myoblast proliferation and that AA is a stimulator of bovine myoblast differentiation. This project also indicates that the proteasome plays a positive role in bovine myoblast differentiation and fusion, and that it does so perhaps by reducing the accumulation of the ID1 protein.
Ph. D.
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44

Ho, Sze-yuen. "Genetic, lipidic and proteomic characterization of an arachidonic acid producing fungus, Mortierella alpina." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290926.

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45

Angelova, Plamena. "Oxidative modulation of transient potassium current by arachidonic acid in brain central neurons." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2007. http://dx.doi.org/10.18452/15671.

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Der neuronale Zelluntergang bei einer Vielzahl von Krankheiten des ZNS, wie z.B. Morbus Alzheimer (AD) und Temporallappenepilepsie (TLE), wird mit oxidativem Stress sowie Fehlfunktionen von Kaliumkanälen in Verbindung gebracht. In dieser Studie soll die selektive neuronale Sensitivität auf oxidativen Stress durch die Messung der oxidativen Modulation von Kaliumströmen untersucht werden. Dabei werden sternförmige Neuronen der zweiten Schicht des entorhinalen Kortex (EC) (bei AD bereits früh geschädigt) mit pyramidalen Neuronen der dritten Schicht des EC (früh geschädigt bei TLE) sowie hippocampalen pyramidalen Neuronen der CA1 Region (bei AD und TLE erst spät geschädigt) miteinander verglichen. Mittels patch-clamp Ganzzellmessung zeigt diese Studie die differentielle Hemmung spannungsabhängiger transienter (IA) und „delayed-rectifier“ K+-Ströme (IK(V)) durch Arachidonsäure (AA) und Wasserstoffperoxid (H2O2). Die intrazelluläre Applikation von AA (1 pM) reduzierte IA in Neuronen des entorhinalen Kortex signifikant stärker verglichen mit Neuronen des CA1. ETYA imitiert diesen Effekt, dies schliesst die Metabolite der AA als Mediatoren des Effekts auf Kaliumkanäle aus. Weder AA noch ETYA reduzierten IK(V). Im Gegensatz dazu reduzierte H2O2 IA in Neuronen des CA1 effektiver als in Neuronen der Schichten II und III des entorhinalen Kortex. Die Reduktion des IA, vermittelt durch AA, wurde durch Radikalfänger (Glutathion, Ascorbinsäure, Vitamin E Analogon Trolox) blockiert. Dabei verstärkten manche dieser Antioxidantien den Effekt der AA, dies legt eine komplexere Modulation dieser Ströme in Schnitten verglichen mit Kulturen nahe. Dies sollte bei der Entwicklung antioxidativer Therapien von AD und TLE berücksichtigt werden. Bei der heterologer Expression von Kv1.4 und Kv4.2 in HEK-293 Zellen wurden funktionelle Kanäle gebildet und A-Typ Ströme ausgelöst. Diese Ströme wurden nach der Applikation von 1 pM AA stark reduziert. ROS scheinen neben ihrer zellschädigenden Wirkung physiologische Prozesse zu regulieren, indem sie eine Reihe von Signalwegen beeinflussen. Da spannungsabhängige Kaliumkanäle vielen wichtigen zellulären Funktionen zugrundeliegen, könnte die Modulation dieser Kanäle durch ROS einen Mechanismus für die Feinabstimmung zellulärer Prozesse darstellen.
Oxidative stress and dysfunction of potassium channels are believed to play a role in neuronal death in a number of CNS diseases (e.g. Alzheimer’s disease, epilepsy). The present study addresses selective neuronal vulnerability to oxidative stress by studying oxidative modulation of potassium channels in entorhinal cortex (EC) layer II stellate neurons (cell loss early in AD) and layer III pyramidal neurons (early damage in TLE), in comparison to hippocampal CA1 pyramidal neurons (late damage in TLE and AD). Using whole-cell patch-clamp, differential inhibition of transient IA and delayed rectifier K+-currents IK(V) by arachidonic acid (AA) and H2O2 was demonstrated. Intracellular AA (1 pM) reduced IA in EC neurons significantly stronger than in CA1 neurons. AA affected the voltage dependence of steady-state inactivation as well. ETYA mimicked the effect of AA, excluding its metabolites as mediators of IA modulation. Neither AA nor ETYA reduced IK(V). In contrast, a non-lipid oxidizing agent, H2O2 reduced IA more effectively and robustly attenuated IK(V) in CA1, compared to EC neurons. AA-mediated reduction of IA was blocked by free radical scavengers (glutathione, ascorbic acid, Trolox). Antioxidants did not simply inhibit AA and H2O2 effects. In particular, they even enhanced AA effects, suggesting more complex modulation of these currents in slices, compared to culture. Moreover, intracellular antioxidants, themselves, influenced maximal conductance and voltage-conductance characteristics of IA and IK(V). This should be considered in design of anti-oxidative therapies in AD and TLE. Heterologous expression of Kv1.4 and of Kv4.2 cDNA in HEK-293 cells formed functional channels and elicited A-type currents, which shared similar biophysical characteristics with native IA from the hippocampus. These currents were strongly decreased upon administration of 1pM AA, demonstrating that at least one of multiple sites for AA action is situated on the pore-forming alfa-subunit of the A-channel. In conclusion, beside contribution to cell damage, ROS may regulate physiological processes by acting on different signalling pathways. Since voltage-gated K+-channels underlie many important cellular functions modulation of these channels by ROS would represent a mechanism for fine tuning of cellular processes.
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46

Cho, Hye-kyung. "Cloning, expression, and fatty acid regulation of mammalian [delta]-5 and [delta]-6 desaturases /." Digital version accessible at:, 1999. http://wwwlib.umi.com/cr/utexas/main.

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Thesis (Ph. D.)--University of Texas at Austin, 1999.
Vita. Greek alphabet delta in title. Includes bibliographical references (leaves 136-155). Available also in a digital version from Dissertation Abstracts.
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Barbieri, Bruno. "Novel aspects of p-aminobenzoic acid metabolism in connection with arachidonic acid oxidation in human lymphoid cells and platelets /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2679-4.

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48

Greco, Nicholas James. "Arachidonic acid metabolism in the platelets and neutrophils of diabetic rabbit and human subjects /." The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487261919110507.

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49

Baker, Nancy Carol. "The Associations Among Dietary Fatty Acids, Plasma Fatty Acids, and Clinical Markers in Postmenopausal Women with Diabetes." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1253666943.

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50

Abdel, Baset Heba. "Characterization of arachidonic acid metabolizing enzymes in the metazoa Schistosoma mansoni and Caenorhabditis elegans." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0023/NQ50097.pdf.

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