6-Ketoprostaglandin F1 alpha: The physiologically active and stable hydrolysis product of EPOPROSTENOL. Found in nearly all mammalian tissue.Thromboxane B2: A stable, physiologically active compound formed in vivo from the prostaglandin endoperoxides. It is important in the platelet-release reaction (release of ADP and serotonin).Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase.Epoprostenol: A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension (HYPERTENSION, PULMONARY).15-Oxoprostaglandin 13-Reductase: (5Z)-(15S)-11 alpha-Hydroxy-9,15-dioxoprostanoate:NAD(P)+ delta(13)-oxidoreductase. An enzyme active in prostaglandin E and F catabolism. It catalyzes the reduction of the double bond at the 13-14 position of the 15-ketoprostaglandins and uses NADPH as cofactor. EC 1.3.1.48.Prostaglandins: A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.Alligators and Crocodiles: Large, long-tailed reptiles, including caimans, of the order Loricata.Prostaglandins F: (9 alpha,11 alpha,13E,15S)-9,11,15-Trihydroxyprost-13-en-1-oic acid (PGF(1 alpha)); (5Z,9 alpha,11,alpha,13E,15S)-9,11,15-trihydroxyprosta-5,13-dien-1-oic acid (PGF(2 alpha)); (5Z,9 alpha,11 alpha,13E,15S,17Z)-9,11,15-trihydroxyprosta-5,13,17-trien-1-oic acid (PGF(3 alpha)). A family of prostaglandins that includes three of the six naturally occurring prostaglandins. All naturally occurring PGF have an alpha configuration at the 9-carbon position. They stimulate uterine and bronchial smooth muscle and are often used as oxytocics.Dinoprost: A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Hypertension, Pulmonary: Increased VASCULAR RESISTANCE in the PULMONARY CIRCULATION, usually secondary to HEART DISEASES or LUNG DISEASES.Platelet Activation: A series of progressive, overlapping events, triggered by exposure of the PLATELETS to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug.Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.Prostaglandins I: A class of cyclic prostaglandins that contain the 6,9-epoxy bond. Endogenous members of this family are biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES.Thromboxane A2: An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).Thromboxane-A Synthase: An enzyme found predominantly in platelet microsomes. It catalyzes the conversion of PGG(2) and PGH(2) (prostaglandin endoperoxides) to thromboxane A2. EC 5.3.99.5.Receptors, Thromboxane: Cell surface proteins that bind THROMBOXANES with high affinity and trigger intracellular changes influencing the behavior of cells. Some thromboxane receptors act via the inositol phosphate and diacylglycerol second messenger systems.Receptors, Thromboxane A2, Prostaglandin H2: A subclass of eicosanoid receptors that have specificity for THROMBOXANE A2 and PROSTAGLANDIN H2.Testosterone: A potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.Lingual Frenum: MUCOUS MEMBRANE extending from floor of mouth to the under-surface of the tongue.Reptiles: Cold-blooded, air-breathing VERTEBRATES belonging to the class Reptilia, usually covered with external scales or bony plates.Keto AcidsWest Indies: Islands lying between southeastern North America and northern South America, enclosing the Caribbean Sea. They comprise the Greater Antilles (CUBA; DOMINICAN REPUBLIC; HAITI; JAMAICA; and PUERTO RICO), the Lesser Antilles (ANTIGUA AND BARBUDA and the other Leeward Islands, BARBADOS; MARTINIQUE and the other Windward Islands, NETHERLANDS ANTILLES; VIRGIN ISLANDS OF THE UNITED STATES, BRITISH VIRGINI ISLANDS, and the islands north of Venezuela which include TRINIDAD AND TOBAGO), and the BAHAMAS. (From Webster's New Geographical Dictionary, 1988, p1330)Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).Endometriosis: A condition in which functional endometrial tissue is present outside the UTERUS. It is often confined to the PELVIS involving the OVARY, the ligaments, cul-de-sac, and the uterovesical peritoneum.Infertility, Female: Diminished or absent ability of a female to achieve conception.Dyspareunia: Recurrent genital pain occurring during, before, or after SEXUAL INTERCOURSE in either the male or the female.Menstruation: The periodic shedding of the ENDOMETRIUM and associated menstrual bleeding in the MENSTRUAL CYCLE of humans and primates. Menstruation is due to the decline in circulating PROGESTERONE, and occurs at the late LUTEAL PHASE when LUTEOLYSIS of the CORPUS LUTEUM takes place.Pelvic Pain: Pain in the pelvic region of genital and non-genital origin and of organic or psychogenic etiology. Frequent causes of pain are distension or contraction of hollow viscera, rapid stretching of the capsule of a solid organ, chemical irritation, tissue ischemia, and neuritis secondary to inflammatory, neoplastic, or fibrotic processes in adjacent organs. (Kase, Weingold & Gershenson: Principles and Practice of Clinical Gynecology, 2d ed, pp479-508)Uterine Diseases: Pathological processes involving any part of the UTERUS.Fallopian Tube Diseases: Diseases involving the FALLOPIAN TUBES including neoplasms (FALLOPIAN TUBE NEOPLASMS); SALPINGITIS; tubo-ovarian abscess; and blockage.Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.Iothalamic Acid: A contrast medium in diagnostic radiology with properties similar to those of diatrizoic acid. It is used primarily as its sodium and meglumine (IOTHALAMATE MEGLUMINE) salts.Vascular Resistance: The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.Glomerular Filtration Rate: The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to INULIN clearance.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Hemostasis: The process which spontaneously arrests the flow of BLOOD from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements (eg. ERYTHROCYTE AGGREGATION), and the process of BLOOD COAGULATION.Vascular Endothelial Growth Factor A: The original member of the family of endothelial cell growth factors referred to as VASCULAR ENDOTHELIAL GROWTH FACTORS. Vascular endothelial growth factor-A was originally isolated from tumor cells and referred to as "tumor angiogenesis factor" and "vascular permeability factor". Although expressed at high levels in certain tumor-derived cells it is produced by a wide variety of cell types. In addition to stimulating vascular growth and vascular permeability it may play a role in stimulating VASODILATION via NITRIC OXIDE-dependent pathways. Alternative splicing of the mRNA for vascular endothelial growth factor A results in several isoforms of the protein being produced.Vascular Endothelial Growth Factors: A family of angiogenic proteins that are closely-related to VASCULAR ENDOTHELIAL GROWTH FACTOR A. They play an important role in the growth and differentiation of vascular as well as lymphatic endothelial cells.Bleeding Time: Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.Platelet Adhesiveness: The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.Platelet Aggregation: The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.Education, Graduate: Studies beyond the bachelor's degree at an institution having graduate programs for the purpose of preparing for entrance into a specific field, and obtaining a higher degree.History, 19th Century: Time period from 1801 through 1900 of the common era.History, 20th Century: Time period from 1901 through 2000 of the common era.Literature, ModernAnthropology: The science devoted to the comparative study of man.Sexology: This discipline concerns the study of SEXUALITY, and the application of sexual knowledge such as sexual attitudes, psychology, and SEXUAL BEHAVIOR. Scope of application generally includes educational (SEX EDUCATION), clinical (SEX COUNSELING), and other settings.Embalming: Process of preserving a dead body to protect it from decay.

The cyclo-oxygenase-dependent regulation of rabbit vein contraction: evidence for a prostaglandin E2-mediated relaxation. (1/645)

1. Arachidonic acid (0.01-1 microM) induced relaxation of precontracted rings of rabbit saphenous vein, which was counteracted by contraction at concentrations higher than 1 microM. Concentrations higher than 1 microM were required to induce dose-dependent contraction of vena cava and thoracic aorta from the same animals. 2. Pretreatment with a TP receptor antagonist (GR32191B or SQ29548, 3 microM) potentiated the relaxant effect in the saphenous vein, revealed a vasorelaxant component in the vena cava response and did not affect the response of the aorta. 3. Removal of the endothelium from the venous rings, caused a 10 fold rightward shift in the concentration-relaxation curves to arachidonic acid. Whether or not the endothelium was present, the arachidonic acid-induced relaxations were prevented by indomethacin (10 microM) pretreatment. 4. In the saphenous vein, PGE2 was respectively a 50 and 100 fold more potent relaxant prostaglandin than PGI2 and PGD2. Pretreatment with the EP4 receptor antagonist, AH23848B, shifted the concentration-relaxation curves of this tissue to arachidonic acid in a dose-dependent manner. 5. In the presence of 1 microM arachidonic acid, venous rings produced 8-10 fold more PGE2 than did aorta whereas 6keto-PGF1alpha and TXB2 productions remained comparable. 6. Intact rings of saphenous vein relaxed in response to A23187. Pretreatment with L-NAME (100 microM) or indomethacin (10 microM) reduced this response by 50% whereas concomitant pretreatment totally suppressed it. After endothelium removal, the remaining relaxing response to A23187 was prevented by indomethacin but not affected by L-NAME. 7. We conclude that stimulation of the cyclo-oxygenase pathway by arachidonic acid induced endothelium-dependent, PGE2/EP4 mediated relaxation of the rabbit saphenous vein. This process might participate in the A23187-induced relaxation of the saphenous vein and account for a relaxing component in the response of the vena cava to arachidonic acid. It was not observed in thoracic aorta because of the lack of a vasodilatory receptor and/or the poorer ability of this tissue than veins to produce PGE2.  (+info)

Angiotensin II-induced constrictions are masked by bovine retinal vessels. (2/645)

PURPOSE: To unmask the vasoconstricting effect of angiotensin II (Ang II) on retinal smooth muscle by studying its interaction with endothelium-derived paracrine substances. This study focused specifically on determining the changes in vascular diameter and the release of endothelial-derived vasodilators, nitric oxide (NO) and prostaglandin (PG) I2, from isolated retinal microvessels. METHODS: Bovine retinal central artery and vein were cannulated, and arterioles and venules were perfused with oxygenated/heparinized physiological salt solution at 37 degrees C. This ex vivo perfused retinal microcirculation model was used to observe the contractile effects of Ang II on arterioles and venules of different diameters. The NO and PGI2 synthase inhibitors, 1-NOARG and flurbiprofen, respectively, were used to unmask Ang II vasoconstriction; the changes in vascular diameters were then measured. Enzyme immunoassays were used to measure the release of cGMP (an index of NO release) and 6-keto-PG-F1alpha (a stable metabolite of PGI2) from isolated bovine retinal vessels. RESULTS: Topically applied Ang II (10(-10) M to 10(-4) M) caused significant (P < 0.05) arteriolar and venular constrictions in a dose-dependent manner, with the smallest retinal arterioles (7+/-0.2 microm luminal diameter) and venules (12+/-2 microm luminal diameter) significantly more sensitive than larger vessels. After the inhibition of endogenous NO and PGI2 synthesis by 1-NOARG and flurbiprofen, respectively, the vasoconstriction effects of Ang II became more pronounced. Again, the smallest vessels tested were significantly more sensitive, and synthesis of endothelial-derived relaxing factor (EDRF), therefore, may be most important in these vessels. Vasoactive doses of Ang II (10(-10) M to 10(-4) M) caused a dose-dependent increase in the release of NO and PGI2 from isolated bovine retinal vessels, indicating that the increase in EDRF may nullify direct Ang II-induced vasoconstriction. Interestingly, intraluminal administration of Ang II caused only vasodilation. CONCLUSIONS: This study demonstrates that the retinal vascular endothelium acts as a buffer against the vasoconstricting agent Ang II via release of vasodilators NO and PGI2, and the vasoconstriction effects due to Ang II are most prominent in the smallest diameter vessels.  (+info)

Inhibitory effects of copper-aspirin complex on platelet aggregation. (3/645)

AIM: To study the inhibitory effects of copper-aspirin complex (CuAsp) on platelet aggregation. METHODS: With adenosine diphosphate the effects of CuAsp on platelet aggregation in vitro or in vivo were investigated. Radioimmunoassay and fluorophotometry were used to measure thromboxane B2 (TXB2) generation from platelets, the levels of TXB2 and of 6-keto-PGF1 alpha in plasma and the platelet serotonin release reaction. RESULTS: In vitro, CuAsp inhibited arachidonic acid (AA)-induced aggregation (IC50 = 17 mumol.L-1, 95% confidence limits: 9-33 mumol.L-1), the release of 5-HT (IC50 = 19 mumol.L-1, 95% confidence limits: 10-30 mumol.L-1), and TXB2 generation from platelets (P < 0.05). CuAsp 10 mg.kg-1 i.g. selectively inhibited AA-induced aggregation, and increased the 6-keto-PGF1 alpha concentration in plasma while decreased that of TXB2. CONCLUSION: CuAsp, in vitro or in vivo, shows more potent inhibitory effects on AA-induced aggregation than aspirin (Asp), related to the inhibition of platelet cyclooxygenase and the release of active substances from platelets.  (+info)

Prostacyclin synthase gene transfer accelerates reendothelialization and inhibits neointimal formation in rat carotid arteries after balloon injury. (4/645)

Prostacyclin (PGI2), a metabolite of arachidonic acid, has the vasoprotective effects of vasodilation, anti-platelet aggregation, and inhibition of smooth muscle cell proliferation. We hypothesized that an overexpression of endogenous PGI2 may accelerate the recovery from endothelial damage and inhibit neointimal formation in the injured artery. To test this hypothesis, we investigated in vivo transfer of the PGI2 synthase (PCS) gene into balloon-injured rat carotid arteries by a nonviral lipotransfection method. Seven days after transfection, a significant regeneration of endothelium was observed in the arteries transfected with a plasmid carrying the rat PCS gene (pCMV-PCS), but little regeneration was seen in those with the control plasmid carrying the lacZ gene (pCMV-lacZ) (percent luminal circumference lined by newly regenerated endothelium: 87. 1+/-6.9% in pCMV-PCS-transfected vessels and 6.9+/-0.2% in pCMV-lacZ vessels, P<0.001). BrdU staining of arterial segments demonstrated a significantly lower incorporation in pCMV-PCS-transfected vessels (7. 5+/-0.3% positive nuclei in vessel cells) than in pCMV-lacZ (50. 7+/-9.6%, P<0.01). Moreover, 2 weeks after transfection, the PCS gene transfer resulted in a significant inhibition of neointimal formation (88% reduction in ratio of intima/media areas), whereas medial area was similar among the groups. Arterial segments transfected with pCMV-PCS produced significantly higher levels of 6-keto-PGF1alpha, the main metabolite of PGI2, compared with the segments transfected with pCMV-lacZ (10.2+/-0.55 and 2.1+/-0.32 ng/mg tissue for pCMV-PCS and pCMV-placZ, P<0.001). In conclusion, this study demonstrated that an in vivo PCS gene transfer increased the production of PGI2 and markedly inhibited neointimal formation with accelerated reendothelialization in rat carotid arteries after balloon injury.  (+info)

Effects of specific inhibition of cyclooxygenase-2 on sodium balance, hemodynamics, and vasoactive eicosanoids. (5/645)

Conventional nonsteroidal anti-inflammatory drugs inhibit both cyclooxygenase (Cox) isoforms (Cox-1 and Cox-2) and may be associated with nephrotoxicity. The present study was undertaken to assess the renal effects of the specific Cox-2 inhibitor, MK-966. Healthy older adults (n = 36) were admitted to a clinical research unit, placed on a fixed sodium intake, and randomized under double-blind conditions to receive the specific Cox-2 inhibitor, MK-966 (50 mg every day), a nonspecific Cox-1/Cox-2 inhibitor, indomethacin (50 mg t.i.d.), or placebo for 2 weeks. All treatments were well tolerated. Both active regimens were associated with a transient but significant decline in urinary sodium excretion during the first 72 h of treatment. Blood pressure and body weight did not change significantly in any group. The glomerular filtration rate (GFR) was decreased by indomethacin but was not changed significantly by MK-966 treatment. Thromboxane biosynthesis by platelets was inhibited by indomethacin only. The urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto prostaglandin F1alpha was decreased by both MK-966 and indomethacin and was unchanged by placebo. Cox-2 may play a role in the systemic biosynthesis of prostacyclin in healthy humans. Selective inhibition of Cox-2 by MK-966 caused a clinically insignificant and transient retention of sodium, but no depression of GFR. Inhibition of both Cox isoforms by indomethacin caused transient sodium retention and a decline in GFR. Our data suggest that acute sodium retention by nonsteroidal anti-inflammatory drugs in healthy elderly subjects is mediated by the inhibition of Cox-2, whereas depression of GFR is due to inhibition of Cox-1.  (+info)

In vitro prostanoid release from spinal cord following peripheral inflammation: effects of substance P, NMDA and capsaicin. (6/645)

1. Spinal prostanoids are implicated in the development of thermal hyperalgesia after peripheral injury, but the specific prostanoid species that are involved are presently unknown. The current study used an in vitro spinal superfusion model to investigate the effect of substance P (SP), N-methyl-d-aspartate (NMDA), and capsaicin on multiple prostanoid release from dorsal spinal cord of naive rats as well as rats that underwent peripheral injury and inflammation (knee joint kaolin/carrageenan). 2. In naive rat spinal cords, PGE2 and 6-keto-PGF1alpha, but not TxB2, levels were increased after inclusion of SP, NMDA, or capsaicin in the perfusion medium. 3. Basal PGE2 levels from spinal cords of animals that underwent 5-72 h of peripheral inflammation were elevated relative to age-matched naive cohorts. The time course of this increase in basal PGE2 levels coincided with peripheral inflammation, as assessed by knee joint circumference. Basal 6-keto-PGF1alpha levels were not elevated after injury. 4. From this inflammation-evoked increase in basal PGE2 levels, SP and capsaicin significantly increased spinal PGE2 release in a dose-dependent fashion. Capsaicin-evoked increases were blocked dose-dependently by inclusion of S(+) ibuprofen in the capsaicin-containing perfusate. 5. These data suggest a role for spinal PGE2 and NK-1 receptor activation in the development of hyperalgesia after injury and demonstrate that this relationship is upregulated in response to peripheral tissue injury and inflammation.  (+info)

Effects of dl-3-n-butylphthalide on production of TXB2 and 6-keto-PGF1 alpha in rat brain during focal cerebral ischemia and reperfusion. (7/645)

AIM: To study the effects of dl-3-n-butylphthalide (NBP) on the changes of thromboxane B2 (TXB2) and 6-keto-PGF1 alpha (6-keto-PGF1 alpha) contents in hippocampus, striatum, and cerebral cortex of rats subjected to focal cerebral ischemia followed by reperfusion. METHODS: Focal cerebral ischemia was induced by inserting a nylon suture into intracranial segment of internal carotid artery from external carotid artery and blockade of the origin of middle cerebral artery. For reperfusion, the suture was pulled out to restore the blood flow to the ischemic brain. Determination of TXB2 and 6-keto-PGF1 alpha was performed by RIA method. RESULTS: Reperfusion following focal cerebral ischemia resulted in increases in TXB2 at 5 min and 6-keto-PGF1 alpha at 30 min and a decrease in the ratio of epoprostenol (PGI2)/thromboxane A2 (TXA2) (6-keto-PGF1 alpha/TXB2) at 5 min in hippocampus, striatum, and cerebral cortex. NBP 10 mg.kg-1 reduced the content of TXB2 without decreasing effect on 6-keto-PGF1 alpha. NBP 20 mg.kg-1 reduced both TXB2 and 6-keto-PGF1 alpha in lesser extent than aspirin (Asp, 20 mg.kg-1). NBP 20 or 10 mg.kg-1 elevated the ratio of PGI2/TXA2 after reperfusion, but Asp 20 mg.kg-1 did not increase the ratio except in striatum at 5 min after reperfusion. CONCLUSION: NBP increases the ratio of PGI2/TXA2 which may have beneficial effects on the impaired microcirculation in postischemic brain tissues.  (+info)

Effects of recombinant human endothelial-derived interleukin-8 on hemorrhagic shock in rats. (8/645)

AIM: To study the effects of recombinant human endothelial-derived interleukin-8 (IL-8) on hemorrhagic shock. METHODS: A profound hemorrhagic shock in rats was produced by exsanguination from femoral artery with mean arterial blood pressure (MABP) maintained at 5.32 kPa for 90 min. After transfusion, IL-8 250 micrograms.kg-1 was i.v. injected. Plasma endothelin-1 (ET-1) and 6 ketoprostaglandin F1 alpha (6-KPGF1 alpha) contents were determined with radioimmunoassay. RESULTS: After i.v. IL-8, the MABP in IL-8 group was elevated obviously (P < 0.01), the rat survival 2 h after infusion was increased (P < 0.05). During profound shock the plasma ET-1 levels were higher (21 +/- 4 vs 8.2 +/- 1.8 ng.L-1, P < 0.01) and the plasma 6-KPGF1 alpha contents lower than those in normal rats (107 +/- 12 vs 157 +/- 11 ng.L-1, P < 0.01). IL-8 remarkably reduced the plasma ET-1 levels (10 +/- 4 ng.L-1, P < 0.01) and enhanced plasma 6-KPGF1 alpha contents (368 +/- 16 ng.L-1, P < 0.01). CONCLUSION: IL-8 has beneficial antishock effects.  (+info)

1. We studied the effect of oral administration of acetylsalicylic acid (1200 mg/day for 3 days) on the urinary excretion of 6-ketoprostaglandin F1α in normal human subjects as an index of prostacyclin production in vivo.. 2. The concentrations and excretion rate in urine fell to 45% of pretreatment levels in 3 days, but returned to pretreatment values after 7 days.. 3. These results suggest that production of prostacyclin in vivo is only partially inhibited by high doses of aspirin and that there are sites of production of prostacyclin which are protected from inhibition by aspirin and which contribute to urinary 6-ketoprostaglandin F1α. The measurement of 6-ketoprostaglandin F1α in urine may therefore be of only limited value as an index of the metabolism of vascular tissue in vivo.. ...
... ,PGF1α-d4 contains 4 deuterium atoms at the 3, 3, 4, and 4 positions. It is intended for use as an internal standard for the quantification of PGF1α by GC- or LC-mass spectrometry.,biological,biology supply,biology supplies,biology product
Creative-Proteomics offer cas 363-23-5 13,14-dihydro-15-keto Prostaglandin E2-d4. We are specialized in manufacturing Stabel Isotope Labeled Analytical Standard products.
However, Devils claw extracts were not as effective as indomethacin, nor were they as effective when given by mouth as when given by injection, apparently due to inactivation iii. Human data: In normal volunteers, three weeks of daily treatment with 2 grams of standardized Devils claw extract had no impact on levels of prostaglandin E2, thromboxane B2, leukotriene B4, or 6-ketoprostaglandin F30. In 13 arthritic patients treated for 13 weeks with Devils claw tablets (410 mg TID) there were no significant improvements28. In an open trial in 630 adults with joint pain, six months of treatment with Devils claw extract in daily dosages of 1 - 3 gms TID resulted in pain relief in 42% - 85% (depending on site of pain); the only adverse effect was mild stomach upset even In a double blind study of adults with joint pain, treatment with 770 mg TID of a standardized Devils Claw extract resulted in significant improvement in pain and flexibility over two months; no side effects were reported4,31. In ...
To elucidate the role of the phosphoinositide signal transduction system in endothelial endothelial prostacyclin production, endothelial cells from human umbilical veins previously labelled with 3H-inositol were incubated with thrombin or histamine. Water-soluble inositol phosphates were separated on anion exchange columns. Both agonists evoked transient bursts of inositol phosphate production with inositol trisphosphate peaking at 15 seconds in histamine-stimulated cells and at 60 seconds in thrombin-stimulated cells. The inositol phosphate production was closely linked to prostacyclin production. After stimulation, there was concurrent desensitization to prostacyclin production and formation of inositol phosphates. Arachidonic acid and the Ca2+-ionophore A23187 did not affect inositol phosphate production in concentrations sufficient to increase prostacyclin production 20-fold, and they did not affect desensitization to a subsequent thrombin stimulation. The phorbol ester 12-o-tetradecanoyl ...
Cyclosporine induces hypertension and wide-spread vasoconstriction after transplantation in addition to reducing kidney function. We studied hemodynamic, renal, and hormonal effects of monotherapy with nifedipine XL (n = 37) in liver transplant recipients within a year after transplant (median, 4.4 months). Systemic hemodynamics were determined with thoracic electrical bioimpedance. Blood pressure before therapy was 172 +/- 4/108 +/- 2 mm Hg. Sixty-four percent of recipients achieved blood pressures less than 140/90 mm Hg mediated by a fall in systemic vascular resistance index (2427 +/- 245 dyne.s.cm-5.m-2 in responders versus 2905 +/- 281 in nonresponders, P , .01). Despite the fall in systemic vascular resistance, glomerular filtration rates were not changed during nifedipine therapy, as measured by both creatinine and iothalamate clearances. Urinary prostacyclin (6-ketoprostaglandin F1 alpha) was suppressed below normal from 2468 +/- 323 ng/d before transplant to 1103 +/- 99 ng/d (P , .01) ...
Title: Implications of the Molecular Basis of Prostacyclin Biosynthesis and Signaling in Pharmaceutical Designs. VOLUME: 12 ISSUE: 8. Author(s):Ke-He Ruan and Jean-Michel Dogne. Affiliation:Division of Hematology,Department of Internal Medicine, University of Texas Health ScienceCenter at Houston, 6431 Fannin St., Houston, Texas 77030, USA.. Keywords:Prostacyclin, Prostaglandin I2, PGI2, Cyclooxygenase-1, COX-1, Cyclooxygenase-2, COX-2, Cytochrome P450, G-protein Coupling Receptor. Abstract: Prostacyclin (PGI2) is one of the major vascular protectors against thrombosis and vasoconstriction, caused by thromboxane A2. Understanding the molecular mechanisms of PGI2 biosynthesis and signaling is crucial to the development of therapeutic approaches to regulate PGI2 functions. This review provides information regarding the most current advances in the findings of the molecular mechanisms for PGI2 biosynthesis in the endoplasmic reticulum (ER) membrane through the coordination between PGI2 synthase and ...
Approach and Results-Type 2 diabetic mice with mutated toll-like receptor 4 (DWM) were protected from hyperglycemia and hypertension, despite an increased body weight. Isometric tension was measured in arterial rings with endothelium. Relaxations to acetylcholine were blunted in aortae and mesenteric arteries of Leprdb/db mice, but not in DWM mice; the endothelial NO synthase dimer/monomer ratio and endothelial NO synthase phosphorylation levels were higher in DWM preparations. These differences were abolished by apocynin. Contractions to acetylcholine (in the presence of L-NAME) were larger in carotid arteries from Leprdb/db mice than from DWM mice and were inhibited by indomethacin and SC560, demonstrating involvement of cyclooxygenase-1. The release of 6-ketoprostaglandin F1α was lower in DWM mice arteries, implying lower cyclooxygenase-1 activity. Apocynin, manganese(III) tetrakis(1-methyl-4-pyridyl) porphyrin, catalase, and diethyldithiocarbamate inhibited endothelium-dependent ...
TY - JOUR. T1 - Prostacyclin, thromboxane A2, and atherosclerosis in young hypercholesterolemic swine. AU - Norman, J. F.. AU - Miller, C. W.. PY - 1994/10. Y1 - 1994/10. N2 - Plasma 6-keto-prostaglandin F1α and thromboxane B2 levels were determined to evaluate their role as predictive indicators for the development and progression of coronary atherosclerosis in young hypercholesterolemic swine. 32 young swine were randomly assigned to the control or atherogenic diet group for 10, 30, 90, or 180 days. Lipid profiles were obtained at the onset and repeated throughout the study. Radioimmunoassays of plasma 6-keto-prostaglandin F1α and thromboxane B2 were recorded at 10 day intervals in the 10 and 30 day subjects and at 30 day intervals in the 90 and 180 day subjects. Sections from the proximal left anterior descending coronary artery were classified based on their histological evidence of atherosclerosis by light microscopy. Hypercholesterolemia was positively correlated with development of ...
Effect of ozone exposure on prostacyclin synthesis in lung.: The effect of ozone exposure on prostacyclin (PGI2) synthesis in the rat lung was studied. Male Wis
Evidence that 13-14 di-hydro, 15-keto prostaglandin D(2)-induced airway eosinophilia in guinea-pigs is independent of interleukin-5. - C J Whelan
The molecular mechanisms of the vascular effects of phytoestrogens are poorly studied. Prostacyclin is a potent vasodilator synthesized by two isoforms of cyclooxygenase (COX) in endothelium. This study examine the effects of two phytoestrogens, the isoflavones genistein and daidzein, on prostacyclin production by cultured human umbilical vein endothelial cells (HUVECs) and the possible role of not only estrogen receptors but also both COX isoforms. The two phytoestrogens significantly increased prostacyclin release in a time- and dose-dependent (0.01-1 μM) manner, being higher than control after 24 h. Selective inhibitors of COX-1, SC-560 [5-(4-chlorophenyl)-1-(4-methoxypjenyl)-3-(trifluoromethyl)-1H-pyrazole], and COX-2, NS-398 (N-[2-(cyclohexyloxy)-4 nitrophenyl]-methanesulfonamide), were used to investigate the relative contribution of each enzyme. Both inhibitors decreased basal production of prostacyclin, but only COX-2 inhibition completely abolished the isoflavone-stimulated ...
Angiotensin-converting enzyme inhibitors (ACEI) block degradation of bradykinin, and bradykinin stimulates prostacyclin synthesis. Therefore, we set out to determine whether the effects of ACE inhibitors on prostaglandin production in essential hypertensive patients are class effects or are dependent on ACE inhibitor structure. In addition, we studied whether hypertensives show an impaired capacity to synthesize vasodilator prostaglandins. To address these questions, we compared the effects of captopril (sulfhydryl-containing inhibitor), enalapril and ramipril (carboxyl-containing inhibitors) and fosinopril (phosphoryl-containing inhibitor) on blood pressure and urinary excretion of 6-keto-prostaglandin (PG) F1-alpha (the breakdown product of prostacyclin) in 44 mild-to-moderate essential hypertensive subjects before and 8 weeks after administration of an ACEI. We also studied prostacyclin excretion in 15 normotensive healthy controls. Levels of urinary 6-keto-PGF1-alpha (pg/ml) were measured by ...
Vasoactive prostanoids may be involved in persistent pulmonary hypertension (PPH) in infants with a congenital diaphragmatic hernia (CDH). We hypothesized that increased levels of prostanoids in bronchoalveolar lavage (BAL) fluid would predict clinical outcome. We measured the concentrations of 6-keto-prostaglandin F(1alpha) (6-keto-PGF(1alpha)), thromboxane B(2) (TxB(2)), protein, albumin, total cell count ...
Prostacyclin molecule. Computer model showing the structure of the hormone prostacyclin, or prostaglandin I2 (PGI2). Atoms are colour-coded (carbon: dark grey, hydrogen: light grey, oxygen: red). Prostacyclin acts to widen blood vessels (thus lowering blood pressure) and to prevent aggregation of platelets (preventing blood clotting). These effects are the opposite of those of the related hormone thromboxane, and the balance between the two is important in regulating the functioning of the circulatory system. When taken as a drug it is known as epoprostenol. - Stock Image C003/3311
The effect of the selective thromboxane A2 synthetase inhibitor OKY-1581, a pyridine derivative [sodium (E)-3-(4-(3-pyridylmethyl)phenyl)-2-methyl-2-propenoate], on thromboxane B2 and 6-keto-prostaglandin F1 alpha levels and platelet aggregation was studied in human volunteers. To clarify its effectiveness as an enzyme inhibitor, OKY-1581, at doses of 17, 83, 167, 417, 833, and 1667 micrograms/kg (n = 5 for each group), was injected intravenously, or was infused (10 micrograms/kg/min; n = 5) over 3 hr on 3 successive days. OKY-1580 (OKY-1581 free acid) was rapidly converted to its main beta-oxidized product, OKY-1565, and its reduced form, OKY-1558. During the study, plasma thromboxane B2 levels, inhibition of thromboxane B2 production in serum, and inhibition of rabbit platelet thromboxane A2 synthetase were monitored continuously. Twenty-five minutes after the injection of the above doses, plasma thromboxane B2 levels decreased by 4 +/- 7%, 40 +/- 14%, 57 +/- 7%, 68 +/- 6%, 93 +/- 5%, and 96 ...
Solute carrier organic anion transporter family member 2A1 (OATP2A1, encoded by the SLCO2A1 gene), which was initially identified as prostaglandin transporter (PGT), is expressed ubiquitously in tissues and mediates the distribution of prostanoids, such as PGE, PGF, PGDand TxB. It is well known to play a key role in the metabolic clearance of prostaglandins, which are taken up into the cell by OATP2A1 and then oxidatively inactivated by 15-ketoprostaglandin dehydrogenase (encoded by HPGD); indeed, OATP2A1-mediated uptake is the rate-limiting step of PGEcatabolism. Consequently, since OATP2A1 activity is required for termination of prostaglandin signaling via prostanoid receptors, its inhibition can enhance such signaling. Read More ...
Abstract: Arachidonic acid and PAF are released from the lungs during anaphyIaxis. The aim of this study is to describe the kinetics of the release of eicosanoids and to observe the effects of selected ihhibitors and a PAF antagonist on their release. Isolated lungs of previously sensitized animals were perfused via the pulmonary artery and challenged with ovalbumin. Prostaglandin E21 throraboxane B2, 6-keto prostaglandin F1? levels were determined in aliquots of effluents with radioimmunoassay and/or enzyme immunoassay techniques whereas leukotrienes B4 and D4 were measured by reverse-phase high performance liquid chromatography. In selected experiments 12-HHT and 12-keto HT were measured in the lung effluents. The peak release of eicosanoids from the lungs ensued approximately at 4-6 minutes after the initiation of anaphylactic shock. Perfusion of the lungs with aspirin, indomethacin decreased the formation of cyclooxygenase products and there was no significant change in the release of LTB4, ...
Plasma 13,14-dihydro-15-keto-prostaglandin F2a (PGFM) levels were measured in patients with twin pregnancies in some of whom the cervix was dilated and effaced.
The first known patent to use energy from ocean waves dates back to 1799, and was filed in Paris by Girard and his son.[13] An early application of wave power was a device constructed around 1910 by Bochaux-Praceique to light and power his house at Royan, near Bordeaux in France.[14] It appears that this was the first oscillating water-column type of wave-energy device.[15] From 1855 to 1973 there were already 340 patents filed in the UK alone.[13]. Modern scientific pursuit of wave energy was pioneered by Yoshio Masudas experiments in the 1940s.[16] He tested various concepts of wave-energy devices at sea, with several hundred units used to power navigation lights. Among these was the concept of extracting power from the angular motion at the joints of an articulated raft, which was proposed in the 1950s by Masuda.[17]. A renewed interest in wave energy was motivated by the oil crisis in 1973. A number of university researchers re-examined the potential to generate energy from ocean waves, ...
Short-term effects of ridogrel, a combined thromboxane synthase inhibitor and receptor antagonist, were investigated in 16 patients with uncomplicated essential hypertension. After a 2-week placebo period without antihypertensive medication, patients were admitted to the hospital overnight on two occasions 3 weeks apart. On each occasion, they received two doses of either placebo or ridogrel (300 mg) 12 hours apart according to a double-blind crossover protocol. Renal and systemic thromboxane A2 and prostacyclin biosynthesis were investigated by measuring urinary excretion of thromboxane B2, 6-oxo-prostaglandin F1 alpha, and their respective 2,3-dinor metabolites using gas chromatography/mass spectrometry. Responses of platelets to a thromboxane A2 mimetic and to adenosine diphosphate were studied turbidometrically. Blood pressure was measured automatically at 20-minute intervals. Ridogrel reduced excretion of 2,3-dinor-thromboxane B2 and thromboxane B2 compared with placebo (21 +/- 6 versus 279 ...
Prostacyclin and hypertension by Gerd Bönner; 1 edition; First published in 1990; Subjects: Drug therapy, Hypertension, Prostaglandins, Therapeutic use
ಕೆಲವು ಮೆನಿಂಗಿಯೊಮಾಸ್ ಪ್ರಕರಣಗಳಲ್ಲಿರುವ ಬುರುಡೆಯಲ್ಲಿ ಅಪರೂಪವಾಗಿರುವ ಗೆಡ್ದೆಗಳನ್ನು ಶಸ್ತ್ರಚಿಕಿತ್ಸೆ ಮೂಲಕ ಯಶಸ್ವಿಯಾಗಿ ತೆಗೆಯಬಹುದು. [೮]ಬಹಳಷ್ಟು ಕಠಿಣ ಪ್ರಕರಣಗಳಲ್ಲಿ ಸ್ಟಿರಿಯಿಟ್ಯಾಕ್ಟಿಕ್ ರೇಡಿಯೊ ಶಸ್ತ್ರಚಿಕಿತ್ಸೆ,ಅಂದರೆ ಗಾಮಾ ಚೂರಿ ಬಳಕೆ,ಸೈಬರ್ ನೈಫ್ ಅಥವಾ ನೊವಿಲಿಸ್ Tx ರೇಡಿಯೊ ಶಸ್ತ್ರಚಿಕಿತ್ಸೆಯು ಅತ್ಯಂತ ಉಪಯುಕ್ತ [೯]ಆಯ್ಕೆಯಾಗಿದೆ. ಬಹಳಷ್ಟು ಪಿಟ್ಯುಟರಿ ಅಡೆನೊಮಾಗಳನ್ನು ಶಸ್ತ್ರಚಿಕಿತ್ಸೆ ಮೂಲಕ ತೆಗೆಯಲಾಗುತ್ತದೆ.ಅಂದರೆ ...
British Atherosclerosis Society. Research Profile. Papers. Cockcroft JR, Ritter JM, Allison DJ, Causon R, Brown MJ. Localisation of extra adrenal catecholamine secreting tumours by selective venous sampling and nuclear magnetic resonance scanning. Postgrad Med J 1987;63:451-453.. Barrow SE, Cockcroft JR, Dollery CT, Hickling NE, Ritter JM. Identification of 13, 14-dihydro-15-oxo-prostaglandin F2 in the circulation during infusions of bradykinin and prostaglandin E2 in man. Br J Pharmacol 1987;81:245-250.. Webb DJ, Benjamin N, Allen MJ, Brown J, OFlynn M, Cockcroft JR. Vascular responses to local atrial natriuretic peptide infusion in man. Br J Clin Pharmacol 1988;26:245-251.. Benjamin N, Cockcroft JR, Collier J, Dollery CT, Ritter JM, Webb DJ. The effect of local converting enzyme inhibition on the vascular responses to angiotensin and bradykinin in the forearm resistance vessels in man. J Physiol 1989;412:543-555.. Cockcroft JR, Allen MJ, Benjamin N, Webb DJ. The effect of local angiotensin ...
Oxidative damage to the vascular endothelium may play an important role in the pathogenesis of atherosclerosis and aging, and may account in part for reduced vascular prostacyclin (PGI2) synthesis associated with both conditions. Using H2O2 to induce injury, we investigated the effects of oxidative damage on PGI2 synthesis in cultured endothelial cells (EC). Preincubation of EC with H2O2 produced a dose-dependent inhibition (inhibitory concentration [IC50] = 35 microM) of PGI2 formation from arachidonate. The maximum dose-related effect occurred within 1 min after exposure although appreciable H2O2 remained after 30 min (30% of original). In addition, H2O2 produced both a time- and dose-dependent injury leading to cell disruption, lactate dehydrogenase release, and 51Cr release from prelabeled cells. However, in dramatic contrast to H2O2 effects on PGI2 synthesis, loss of cellular integrity required doses in excess of 0.5 mM and incubation times in excess of 1 h. The superoxide-generating ...
COX-2 preferentially leads to synthesis of prostacyclin which have anti-platelet aggregation effects. COX-1 preferentially leads to synthesis of thromboxane which induces platelet aggregation. One would then expect COX-1 inhibition to cause more blood-thinning than COX-2 inhibition. This is the reason COX-2 inhibitors are associated with increased risk of cardiovascular events (by inhibiting prostacyclin synthesis without inhibiting thromboxane synthesis). However, Celebrex is not as selective a COX-2 inhibitor as other coxibs such as rofecoxib (which was removed from the market in 2004), and has minor activity against COX-1 ...
Prostacyclin is a steroid that is produced naturally in the body of a healthy person. It causes blood vessels in the lungs to relax and allows blood to flow through them more easily. People with pulmonary hypertension do not produce enough prostacyclin, so the blood vessels in the lungs are constricted. Prostacyclin, also known as epoprostenol, is used to treat this condition. Pulmonary hypertension IS23 Helpline: 03000 030 555 British Lung Foundation 2012 [email protected] Prostacyclin therapy was initially used as a bridge to lung transplantation although it has also emerged as an alternative to transplantation in some patients. Prostacyclin, or its longer lasting derivatives, can be given by continuous infusion and sometimes by other routes. It has been shown to improve breathlessness and probably survival in patients with idiopathic PAH. These are a class of oral drugs that are now licensed for the treatment of Endothelin is a peptide made by the body in the endothelium (a layer of cells ...
Caffeine (10 mM) stimulated the outputs of prostaglandin (PG) F2α, PGE2 and PGI2 (measured as 6-keto-PGF1α) from the day 7 and day 15 guinea-pig uterus superfused in vitro. Caffeine-induced PG production was unaffected by the removal of extracellular calcium, ryanodine (RY) and ruthenium red (inhibitors of calcium release from ryanodine receptor (RYR) channel, and calmodulin inhibitors (W-7 and trifluoperazine (TFP)). In fact, W-7 greatly potentiated the caffeine effect on PGF2α output. TMB-8, an intracellular calcium antagonist, inhibited the increase in PGF2α output produced by caffeine without preventing the increases in outputs of PGE2 and 6-keto-PGF1α. Caffeine (1 mM but not 0.1 mM) and theophylline (Theo.; 10 mM) also stimulated PG outputs from the day 7 guinea-pig uterus superfused in vitro. Caffeine and RY both stimulated prostaglandin production by the perfused mesenteric vascular bed of the rat. Caffeine (10 mM) stimulated the output of PGF2α after 8 h, and the output of ...
Value And Reference Types in C# - ASP.NET. Memory Allocation. Stack and Heap. Call By reference and Call by value. DotNetHints is a blog and forum concerning .Net Asp.Net and web issues.
Members[6][edit]. PROSTACYCLINS Flolan. (epoprostenol sodium). for Injection Continuously infused 2 ng/kg/min to start, ... 12 (9): 470-6. doi:10.1002/bms.1200120905. PMID 2996649.. *^ Johnson, Roy A.; Lincoln, Frank H.; Nidy, Eldon G.; Schneider, ... Inhaled 6-9 times daily 2.5 μg 6-9 times daily to start, increased to 5.0 μg 6-9 times daily if well tolerated Class III. Class ... IL-1, IL-6. ↑IL-10 ↓Proinflammatory cytokines. ↑Antiinflammatory cytokines Antimitogenic ↓VEGF. ↓TGF-β ↓Angiogenesis. ↑ECM ...
15-hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic acid MeSH D10.251.355.255.100.637.100 --- prostaglandins a MeSH ... 15-hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic acid MeSH D10.251.355.255.550.100 --- prostaglandins a MeSH ... alpha-linolenic acid MeSH D10.251.355.450.450 --- gamma-linolenic acid MeSH D10.251.355.840 --- sorbic acid MeSH D10.251. ... alpha-linolenic acid MeSH D10.251.355.310.640.425 --- gamma-linolenic acid MeSH D10.251.355.325 --- fatty acids, ...
15-hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic acid MeSH D23.469.050.175.725.740 --- prostaglandins a MeSH ... 15-hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic acid MeSH D23.469.700.645 --- prostaglandins a, synthetic MeSH ... transforming growth factor alpha MeSH D23.348.479.992.720 --- transforming growth factor beta MeSH D23.348.479.996 --- wnt ... transforming growth factor alpha MeSH D23.348.900.720 --- transforming growth factor beta MeSH D23.469.050.050 --- angiotensins ...
... ,PGF1α-d4 contains 4 deuterium atoms at the 3, 3, 4, and 4 positions. It ... 8-iso-13,14-dihydro-15-keto Prostaglandin F2alpha from Cayman Chemical. 6. Prostaglandin D2 from Cayman Chemical. 7. ... Anti-6-keto Prostaglandin F1 alpha (EIA Antiserum) Antibody, Unconjugated from Cayman Chemical. 2. 15(S)-15-methyl ... 6 bottle (70 mm) rotisserie + shaker tray available for simultaneous use. Includes linear and orbital shaker trays, 4 extra ...
Members[6][edit]. PROSTACYCLINS Flolan. (epoprostenol sodium). for Injection Continuously infused 2 ng/kg/min to start, ... 12 (9): 470-6. doi:10.1002/bms.1200120905. PMID 2996649.. *^ Johnson, Roy A.; Lincoln, Frank H.; Nidy, Eldon G.; Schneider, ... Inhaled 6-9 times daily 2.5 μg 6-9 times daily to start, increased to 5.0 μg 6-9 times daily if well tolerated Class III. Class ... IL-1, IL-6. ↑IL-10 ↓Proinflammatory cytokines. ↑Antiinflammatory cytokines Antimitogenic ↓VEGF. ↓TGF-β ↓Angiogenesis. ↑ECM ...
... platelet alpha-granule release or plasma fibrinogen, compared with placebo. Excretion of 2,3-dinor-6-keto-PGF1 alpha ( ... and increased plasma concentration of the platelet alpha-granule constituents, platelet factor 4 and beta-thromboglobulin, ...
6-Ketoprostaglandin F1 alpha / blood. Arteriosclerosis / blood*, drug therapy. Blood Platelets / drug effects*, metabolism. ...
Next Document: Application of an alpha-sidechain length-specific monoclonal antibody to immunoaffinity purification.... ... 6-Ketoprostaglandin F1 alpha / metabolism. Aged. Alprostadil / metabolism, pharmacology*. Dinoprostone / metabolism. Female. ... In the control group, both 6-keto PF1 alpha and PGE2 showed only a slight increase both during and after the operation. ... 0/Lipid Peroxides; 363-24-6/Dinoprostone; 54397-85-2/Thromboxane B2; 57576-52-0/Thromboxane A2; 58962-34-8/6-Ketoprostaglandin ...
6-Ketoprostaglandin F1 alpha / blood. Clinical Trials as Topic. Double-Blind Method. Fat Emulsions, Intravenous / ... 0/Fat Emulsions, Intravenous; 0/Prostaglandins; 54397-85-2/Thromboxane B2; 58962-34-8/6-Ketoprostaglandin F1 alpha; 7782-44-7/ ...
7218038 - Effect of oxidized fish oil, dl-alpha-tocopheryl acetate and ethoxyquin supplementation.... 7907168 - Role of dietary ... The levels of 6-keto-PGF1 alpha were highest in rats fed the 10% corn oil diet regardless of the tissue assayed. Rats fed the 2 ... 6-Ketoprostaglandin F1 alpha / blood, metabolism. Aging. Animals. Brain / metabolism. Cattle. Corn Oil / administration & ... 0/Dietary Fats; 0/Eicosanoids; 0/Fish Oils; 0/Triglycerides; 363-24-6/Dinoprostone; 58962-34-8/6-Ketoprostaglandin F1 alpha; ...
3474249 - Pre partum milk fat secretion and concentrations of progestins, prostaglandin f2 alpha .... 25466189 - One-pot ... 6-Ketoprostaglandin F1 alpha / analysis, metabolism. Animals. Bicyclo Compounds / pharmacology. Cyclooxygenase 1 / metabolism. ... Mucosal levels of PGE(2) and 6-keto PGF(1a) increased after exposure to TC in all groups of mice. In conclusion, the decrease ... 58962-34-8/6-Ketoprostaglandin F1 alpha; 81-24-3/Taurocholic Acid; EC 1.14.99.-/Ptgs2 protein, mouse; EC 1.14.99.1/ ...
Intravenous infusion of a selective inhibitor of thromboxane A2 synthetase in man: influence on thromboxane B2 and 6-keto- ... prostaglandin F1 alpha levels and platelet aggregation.. Y Yui, R Hattori, Y Takatsu, H Nakajima, A Wakabayashi, C Kawai, N ... Intravenous infusion of a selective inhibitor of thromboxane A2 synthetase in man: influence on thromboxane B2 and 6-keto- ... prostaglandin F1 alpha levels and platelet aggregation.. Y Yui, R Hattori, Y Takatsu, H Nakajima, A Wakabayashi, C Kawai, N ...
Mouse Anti-Human S-100 alpha/beta chain Monoclonal Antibody, Unconjugated, Clone 8B10 from Santa Cruz Biotechnology, Inc.. 11. ... Costar 6 Well Cell Culture Plate, 9.5 cm2, 34.8 mm Diam. Well, Sterile from Sigma-AldrichRabbit Anti-Human ErbB-2, phospho ( ... 6. Mouse Anti-Mouse Glutathione S-transferase M1 (GSTM1) Monoclonal Antibody, Unconjugated from Lifespan Biosciences. 7. Goat ... Anti-6-keto Prostaglandin F1 alpha (EIA Antiserum) Antibody, Unconjugated from Cayman Chemical. 4. Mouse Anti-Amodiaquine ...
II-2B). 6. Obstetric care providers should take BMI into consideration when arranging for fetal anatomic assessment in the ... 3768289 - Vaginal and abdominal delivery increases maternal urinary 6-keto-prostaglandin f1 alpha.... ...
Technetium 99m (m=metastable) which is the decay product of Molybdenum 99, has a half-life of about 6 hours and is used ... Technetium 99m (m=metastable) which is the decay product of Molybdenum 99, has a half-life of about 6 hours and is used ...
214309 - Effects of prostaglandin e2, prostaglandin i2 and 6-keto-prostaglandin f1 alpha on adre.... 7425839 - Dysphagia due to ...
Carlberg M,Nejaty J,Froysa B,Guan Y,Soder O,Bergqvist A. Elevated expression of tumour necrosis factor alpha in cultured ... Sondheimer SJ,Flickinger G. Prostaglandin F2 alpha in the peritoneal fluid of patients with endometriosisInt J FertilYear: ... Accepted Day: 6 Month: 12 Year: 2011. Electronic publication date: Day: 3 Month: 2 Year: 2012. pmc-release publication date: ... 1998, 2002); cytokines such as IL-1, IL-6, IL-8 and IL-10; growth factors, such as vascular endothelial growth factor, nerve ...
... and F2 alpha showed that 6-keto-prostaglandin F1 alpha was the major prostaglandin formed in the microvessels, in the larger ... Choroid plexus and intact surface vessels synthesized 6-keto-prostaglandin F1 alpha at 37 and 35 ng/mg protein/10 min, ... Comparison of the synthesis of prostaglandins 6-keto-F1 alpha, E2, ... 6-keto-prostaglandin F1 alpha, was 11 ng/mg protein/10 min. ... the exogenously added prostaglandin endoperoxides to 6-keto-prostaglandin ...
Urinary prostacyclin (6-ketoprostaglandin F1 alpha) was suppressed below normal from 2468 +/- 323 ng/d before transplant to ...
F1.2, β-TG, and VEGF were measured by using the following commercially available assay kits: Enzygnost F1+2 (Behringwerke AG), ... In vivo measurement of thromboxane B2 and 6-keto-prostaglandin F1 alpha in humans in response to a standardized vascular injury ... 6 7 So far, 4 isoforms of VEGF, with 121, 165, 189, and 206 amino acids, have been identified.8 VEGF121 and VEGF165 are ...
TGF-alpha and TGF-beta(1) expression increased only in lungs of preterm lambs. Tropoelastin mRNA increased more with MV of ... Altered expression of key growth factors (TGF alpha, TGF beta 1, PDGF-A) and flawed formation of alveoli and elastin (Eln) in ... No significant differences were detected for other proteins (inducible NOS, alpha-smooth muscle actin, and pancytokeratin). ... alpha, TGF-beta(1)] and matrix molecules (tropoelastin, fibrillin-1, fibulin-5, lysyl oxidases) that regulate elastin synthesis ...
... we show identical effects of IL-4 on TNF-alpha-induced responses to those observed with endothelial cells of foetal origin [33] ... effects of interferon gamma and interleukin 4 on responses of human vascular endothelial cells to tumour necrosis factor alpha. ... Correlation between umbilical artery resistance index, 6 ketoprostaglandin F1 alpha and thromboxane B2 in the fetoplacental ... Moreover, the umbilical artery Resistance Index was significantly correlated with the 6-keto PGF1 alpha/thromboxane B2 ratio ...
Verapamil inhibited the ischemia-reperfusion-induced increase in 6-keto-PGF1 alpha but did not alter the effect of ischemia- ... We simultaneously determined the rate of release of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) ... Verapamil decreased the baseline values of 6-keto-PGF1 alpha and increased those of TXB2. ...
The latter subsequently catalyzes the reduction of 15-oxo-PGE2 to 15-ketoprostaglandin F2 alpha (15-Keto-PGF2alpha) that is in ... 15-Keto-PGF2 alpha can also be formed from PGF2 alpha via the reaction catalyzed by CBR1 [44] or HPGD [34], [45]. ... There are various ways to form Prostaglandin F2 alpha (PGF2 alpha). One way is by reduction of the PGE2 catalyzed by Carbonyl ... Enzymatic conversion of prostaglandin H2 to prostaglandin F2 alpha by aldehyde reductase from human liver: comparison to the ...
6-Ketoprostaglandin F1 alpha/analysis Animals Cell Transformation, Neoplastic/*genetics/pathology Colorectal Neoplasms/* ...
... is involved in the up-regulation of matrix metalloproteinase-9 in cholangiocarcinoma induced by tumor necrosis factor-alpha. Am ... Simplified assay for the quantification of 2,3-dinor-6-keto-prostaglandin F1 alpha by gas chromatography-mass spectrometry. J ...
Penile aspiration, intracorporeal alpha-agonist injection and unilateral arterial embolization failed to resolve the priapism ... The relationship of penile blood thromboxane B2 and 6-keto-prostaglandin F1 alpha in both psychogenically and arteriogenically ... 6) and nonoiled (mean = 306 mg/100 ml, SD = 87, n = 8) areas of Prince William Sound, Alaska (USA) following the Exxon Valdez ...
  • In the control group, both 6-keto PF1 alpha and PGE2 showed only a slight increase both during and after the operation. (biomedsearch.com)
  • Male BHE/cdb rats, which carry a genetic trait for non-insulin-dependent diabetes mellitus, were fed these diets for 9 mo, at which time their glucose tolerance levels were determined, as were brain, kidney medulla, and plasma levels of PGE2, 6-keto-PGF1 alpha, and LTB4. (biomedsearch.com)
  • The latter subsequently catalyzes the reduction of 15-oxo-PGE2 to 15-ketoprostaglandin F2 alpha ( 15-Keto-PGF2alpha ) that is in turn reduced by CBR1 to PGF2 alpha . (bio-rad.com)
  • Contents of 6-keto-PGF1alpha in bovine aorta endothelial cells, PGE2 in mouse abdominal macrophages, and 6-keto-PGF1alpha in rat stomach tissue were determined. (bvsalud.org)
  • Transdermal nicotine produced plasma levels of nicotine in the same range as those during smoking but had no effect on thromboxane A2 metabolite excretion, platelet alpha-granule release or plasma fibrinogen, compared with placebo. (nih.gov)
  • Glucose 1,6-bisphosphate and the mechanism of the Pasteur effect in diaphragm muscle. (docphin.com)
  • A total of 72 SD rats (3) were randomly divided into 6 groups: sham operation group, cerebral ischemia-reperfusion model group (I/R gourp), low (10 mg.kg-1), middle (20 mg.kg-1) and high (40 mg.kg-1) doses of paeoniflorin groups and nimrnodipine group. (bvsalud.org)
  • OBJECTIVE: To evaluate the efficacy and safety of buphenine, aminophenazone and diphenylpyraline hydrochloride when compared with placebo for the control of symptoms associated with common cold in children 6-24 months of age. (bvsalud.org)
  • One of the steroidal glycosides (6) showed significant cytotoxic activity against gastric cancer SGC7901 and liver cancer BEL-7402 cells. (bvsalud.org)
  • The levels of 6-keto-PGF1 alpha were highest in rats fed the 10% corn oil diet regardless of the tissue assayed. (biomedsearch.com)
  • Statistically significant decreases in TNF-alpha levels after LPS injection were observed either with ozone intraperitoneal applications at 0.2 (78 \%), 0.4 (98.5 \%) and 1.2 (98.6 \%) mg/ kg or by rectal application at 0.2 (46.2 \%) and 0.4 (97.4 \%) mg/kg. (neuekrebstherapie-kleintierpraxis.de)
  • Our aim was to determine if inhibition of NF kappa B alters cell cycle characteristics in hepatocytes treated with tumor necrosis factor alpha (TNF alpha). (saladgaffe.tk)
  • Z. B. Zamora, A. Borrego, O. Y. López, R. Delgado, S. Menéndez, S. Schulz, and F. Hernández, „Inhibition of tumor necrosis factor-alpha release during endotoxic shock by ozone oxidative preconditioning in mice. (neuekrebstherapie-kleintierpraxis.de)
  • The aim of this study was to analyze the effect of ozone oxidative preconditioning on the level of tumor necrosis factor-alpha (TNF-alpha) in the serum of mice treated with lipopolysaccaride (LPS). (neuekrebstherapie-kleintierpraxis.de)
  • Both observational studies ( 1-5 ) and controlled clinical trials ( 6 ) support the concept that aspirin prevents mortality and metastasis from adenocarcinomas. (aacrjournals.org)
  • The effect of combined oral contraceptives containing 158 micrograms of levonorgestrel and 38 micrograms of ethinyl estradiol on vitamin B-1, B-2, B-6, B-12, folates, vitamin A, carotenoids, vitamin E and tryptophan load test was studied in a group of 34 healthy non-lactating women. (saladgaffe.tk)
  • CONCLUSIONS: The results in this study indicates that Flumil is a safe and effective drug for control of symptoms present in the common cold in children aged 6-24 months. (bvsalud.org)
  • SEARCH STRATEGY AND SELECTION CRITERIA References for this review were identified by searches of PubMed from 1966 to February 2008 with the terms migraine, food trigger, alternative treatment, magnesium, coenzyme Q10 (CoQ10), riboflavin, feverfew, alpha lipoic acid, and butterbur. (docplayer.net)
  • Technetium 99m (m=metastable) which is the decay product of Molybdenum 99, has a half-life of about 6 hours and is used diagnostically as a radioactive imaging agent. (curehunter.com)
  • Tuber melanosporum (TM), a valuable edible fungus, contains 19 types of fatty acid, 17 types of amino acid, 6 vitamins, and 7 minerals. (hindawi.com)
  • Patients who underwent hepatic resection were randomly assigned to two groups consisting of a control (n = 5) and a PGE1 treatment group (n = 6). (biomedsearch.com)
  • We also recommend the use of the following supplements in the preventative treatment of migraines, in decreasing order of preference: magnesium, Petasites hybridus, feverfew, coenzyme Q10, riboflavin, and alpha lipoic acid. (docplayer.net)
  • Key Words: migraine, food triggers, magnesium, feverfew, butterbur, riboflavin, coenzyme Q10, alpha lipoic acid, alternative treatment (Clin J Pain 2009;25: ) Migraine is a common and disabling disorder that affects over 28 million Americans. (docplayer.net)
  • Additionally, TM increased the expression of nuclear respiratory factor 2 (Nrf2), catalase, heme oxygenase 1, heme oxygenase 2, and manganese superoxide dismutase 2 and decreased the expression of protein kinase C alpha, phosphor-janus kinase 2, phosphor-signal transducer and activator of transcription 3, and phosphor-nuclear factor- κ B in the kidneys. (hindawi.com)
  • No significant difference was observed in NOx and 6 keto PGFIalpha between the two groups. (bvsalud.org)