The physiologically active and stable hydrolysis product of EPOPROSTENOL. Found in nearly all mammalian tissue.
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).
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.
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).
(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.
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.
Large, long-tailed reptiles, including caimans, of the order Loricata.
(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.
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.
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)
Increased VASCULAR RESISTANCE in the PULMONARY CIRCULATION, usually secondary to HEART DISEASES or LUNG DISEASES.
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.
The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
A class of cyclic prostaglandins that contain the 6,9-epoxy bond. Endogenous members of this family are biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES.
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).
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.
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.
A subclass of eicosanoid receptors that have specificity for THROMBOXANE A2 and PROSTAGLANDIN H2.
A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.
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.
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.
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.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
A plant genus of the family ARISTOLOCHIACEAE. Species of this genus have been used in traditional medicine but they contain aristolochic acid which is associated with nephropathy. These are sometimes called 'snakeroot' but that name is also used with a number of other plants such as POLYGALA; SANICULA; ASARUM; ARISTOLOCHIA; AGERATINA; and others.
Analog or digital communications device in which the user has a wireless connection from a telephone to a nearby transmitter. It is termed cellular because the service area is divided into multiple "cells." As the user moves from one cell area to another, the call is transferred to the local transmitter.
Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
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.
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.
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.
Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.
The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.
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.
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.
Time period from 1801 through 1900 of the common era.
Time period from 1901 through 2000 of the common era.
The science devoted to the comparative study of man.
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.
Process of preserving a dead body to protect it from decay.
Specialized arterial vessels in the umbilical cord. They carry waste and deoxygenated blood from the FETUS to the mother via the PLACENTA. In humans, there are usually two umbilical arteries but sometimes one.
The profession of writing. Also the identity of the writer as the creator of a literary production.
Collections of facts, assumptions, beliefs, and heuristics that are used in combination with databases to achieve desired results, such as a diagnosis, an interpretation, or a solution to a problem (From McGraw Hill Dictionary of Scientific and Technical Terms, 6th ed).
Congenital abnormality where one, instead of the usual two, UMBILICAL ARTERY connects the fetus to the placenta.
The visualization of tissues during pregnancy through recording of the echoes of ultrasonic waves directed into the body. The procedure may be applied with reference to the mother or the fetus and with reference to organs or the detection of maternal or fetal disease.
Venous vessels in the umbilical cord. They carry oxygenated, nutrient-rich blood from the mother to the FETUS via the PLACENTA. In humans, there is normally one umbilical vein.
Ultrasonography applying the Doppler effect, with frequency-shifted ultrasound reflections produced by moving targets (usually red blood cells) in the bloodstream along the ultrasound axis in direct proportion to the velocity of movement of the targets, to determine both direction and velocity of blood flow. (Stedman, 25th ed)

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.. ...
1. The aim of this investigation was to study the role of prostaglandins in the impaired Na+ conservation of the ageing kidney.. 2. We measured the urinary excretion of thromboxane B2, 6-keto-prostaglandin F1α and prostaglandin E2 in young (3-4 months) and old (20-21 months) rats after 12, 24 and 36 h of Na+ deprivation. In a separate protocol, we measured prostanoid synthesis by isolated glomeruli, cortical homogenates, medullary slices and papillary slices from young and old rats in basal conditions and after 15 days of dietary Na+ deprivation.. 3. In the acute study, urinary excretion of 6-ketoprostaglandin F1α and prostaglandin E2 decreased in young but not in old rats. Urinary excretion of prostaglandin E2 was lower in old rats, but did not vary significantly with Na+ deprivation.. 4. In old rats, thromboxane B2 synthesis was increased in all the portions of the kidney except the medulla. Production of 6-keto-prostaglandin F1α was elevated in glomeruli and tended to increase in the ...
6-keto Prostaglandin F1alpha-d4 from Cayman Chemical,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 ...
Catalysis of the reaction: 15-keto-prostaglandin + NAD(P)H + H+ -> 13,14-dihydro-15-keto-prostaglandin + NAD(P)+. This reaction is the reduction of 15-keto-prostaglandin. [EC:1.3.1.48, GOC:mw, KEGG:R04556, KEGG:R04557, PMID:17449869]
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 ...
TY - JOUR. T1 - C-reactive protein decreases prostacyclin release from human aortic endothelial cells. AU - Venugopal, Kumar Senthil. AU - Devaraj, Sridvi. AU - Jialal, Ishwarlal. PY - 2003/10/7. Y1 - 2003/10/7. N2 - Background - In addition to being a risk marker for cardiovascular disease, much recent data suggest that C-reactive protein (CRP) promotes atherogenesis. Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic state. We have shown that CRP decreases endothelial NO synthase expression and bioactivity in human aortic endothelial cells (HAECs). PGI2 is a potent vasodilator and inhibitor of platelet aggregation. Hence, the aim of this study was to examine the effect of CRP on PGI2 release from HAECs and human coronary artery endothelial cells (HCAECs). Methods and Results - HAECs and HCAECs were incubated with human CRP (0 to 50 μg/mL for 24 hours). The release of PGF-1α, a stable product of PGI2, was also assayed in the absence and presence ...
A rat fecal peritonitis model of acute intraabdominal sepsis was investigated in order to evaluate the potential role of arachidonic acid metabolites in septic shock. Immunoreactive (i) Thromboxane (Tx) 8 2 , the stable metabolite of TXA2 and i6-keto-PGF 1a , the stable metabolite of prostacyclin, were measured by radioimmuonassay. plasma levels of iTXB2 rapidly increased from non-detectable (ND,200 pg/ml) to 1,066 -/+ 194 pg/ml (N=14) 1 hour after feces injction. iTxB2 then increased to 1,695 -/+ 218 pg/ml (N=16) at 4 hours and remained unchanged through 6 hours. Plasma i6-keto-PGF1a increased from ND to 3,777 -/+ 414 pg/ml (N=16) at 1 hour. Four hours after feces, i6-keto-PGF1a levels rose to 6,945 -/+ 732 pg/ml (N=16) then continued to rise to 9,465 -/+ 792 pg/ml (N=7) at 6 hours. Either essential fatty acid deficiency (arachidonic acid depletion) or indomethacin pretreatment (cyclooxygenase inhibition) significantly decreased (P,0.01) the elevations of plasma iTxB2 and i6-keto-PGF1a ...
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 ...
PTGIS (prostaglandin I2 (prostacyclin) synthase), Authors: Inês Cebola, Miguel A Peinado. Published in: Atlas Genet Cytogenet Oncol Haematol.
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 ...
Pseudomonas aeruginosa pneumonia causes a vasculitis of small pulmonary arteries. While the fully developed lesion demonstrates vessel wall necrosis, the early lesion is remarkable for preservation of viable endothelium despite vessel wall invasion by bacteria. Pyocyanin, an exoproduct of P. aeruginosa, markedly inhibited prostacyclin production by pulmonary artery endothelial cells without causing cell lysis. Pyocyanin might after vascular homeostasis in the absence of cytolysis.. ...
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 ...
Cultured endothelial cells from human umbilical cord labeled with [3H]20:4 release radiolabel when exposed to leukotrienes C or D (LTC or LTD). The major radiol
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 ...
中文: 经气相色谱分析PGF-为葡聚糖,PGF-、PGF- 和PGF-由葡萄糖、甘露糖和半乳糖组成,摩尔比分别为:. :.、:0. :0.和:0.:0. 8。 更详细... ...
To study whether prostacyclin and thromboxane A2 might play a role in neonatal adaption pieces of the umbilical arteries of infants born vaginally (n = 18) or by elective caesarean section (n = 11) were superfused in vitro and the release of 6-keto-PGF1a (hydration product of prostacyclin) and thromboxane B2 (metabolite of thromboxane A2) measured by radioimmunoassay. In addition, the capacity of fetal platelets to produce thromboxane A2 and the neonatal urinary concentrations of 6-keto-PGF1a were measured. Infants born by caesarean section had lower diastolic blood pressure, higher heart rate, and smaller differences between rectal and skin temperature compared with infants born vaginally during the first two hours of life. The only difference encountered in the prostanoids between the groups was reduced urinary excretion of 6-keto-PGF1a in infants born by caesarean section, whose release of 6-keto-PGF1a by the umbilical artery was positively correlated with heart rate, respiration frequency, ...
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 ...
The Doctors answer a viewers question about bad breath in relation to sinusitis. Ear nose and throat specialist Dr. Andrew Ordon shares bad breath is actually ... ...
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.
12 (9): 470-6. doi:10.1002/bms.1200120905. PMID 2996649. Johnson, Roy A.; Lincoln, Frank H.; Nidy, Eldon G.; Schneider, William ... Prostacyclin, which has a half-life of 42 seconds, is broken down into 6-keto-PGF1, which is a much weaker vasodilator. As ... PGI2 is derived from the ω-6 arachidonic acid. PGI3 is derived from the ω-3 EPA. Prostacyclin can be synthesized from the ... 6 April 2020. Retrieved 22 October 2020. "Flolan- epoprostenol sodium injection, powder, lyophilized, for solution Diluent- ...
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 D10.251 ... alpha-linolenic acid MeSH D10.251.355.450.450 - gamma-linolenic acid MeSH D10.251.355.840 - sorbic acid MeSH D10.251.355.920 - ... alpha-linolenic acid MeSH D10.251.355.310.640.425 - gamma-linolenic acid MeSH D10.251.355.325 - fatty acids, monounsaturated ...
15-hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic acid MeSH D23.469.050.175.725.740 - prostaglandins a MeSH D23.469 ... 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 proteins ... alpha-fetoproteins MeSH D23.101.840.055 - antigens, cd30 MeSH D23.101.840.075 - antigens, tumor-associated, carbohydrate MeSH ...
... ,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 ...
14-dihydro-15-keto-prostaglandin F2 alpha by aminoglutethimide in advanced breast cancer. ... 14-dihydro-15-keto-prostaglandin F2 alpha by aminoglutethimide in advanced breast cancer. ... 14-dihydro-15-keto-prostaglandin F2 alpha by aminoglutethimide in advanced breast cancer. ... 6-Ketoprostaglandin F1 alpha, Aminoglutethimide, Breast Neoplasms, Dinoprost, Female, Humans, Menopause, Middle Aged, ...
6-ketoprostaglandin F1.alpha., prostaglandin I1, and prostaglandin I3". Journal of the American Chemical Society. 100 (24): ...
Cardiopulmonary bypass induces platelet activation and dysfunction, which result in platelet deposition and depletion. Reduced platelet numbers and abnormal platelet function may contribute to postoperative bleeding. A membrane oxygenator may preserve platelets and reduce bleeding more than a bubble …
... 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 ...
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 ...
6,8,10,14-Eicosatetraenoic acid, 5,12-dihydroxy-, (S-(R*,S*-(E,Z,E,Z)))- ...
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 ...
... 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 ...
We determined 6-keto prostaglandin F1 alpha since it is the stable metabolite of the bioactive prostacyclin. MDHM appeared to ... At 4 to 6 h after injection, granulocyte counts began to increase again, whereas lymphocyte counts remained low. No ... MDHM, a macrophage-stimulatory product of Mycoplasma fermentans, leads to in vitro interleukin-1 (IL-1), IL-6, tumor necrosis ... Priming with gamma interferon further increased MDHM-mediated IL-6 release. Since monokines can be pyrogenic, we tested the ...
WistarRenal CirculationReperfusion InjurySensory Receptor CellsTRPV Cation ChannelsTumor Necrosis Factor-alpha ... and tumor necrosis factor-alpha, and decreased renal tissue blood flow. However, pretreatment with CGRP significantly improved ... and tumor necrosis factor-alpha, and decreased renal tissue blood flow. However, pretreatment with CGRP significantly improved ... 6-Ketoprostaglandin F1 alphaAcute DiseaseAnimalsAnti-Inflammatory Agents, Non-SteroidalCalcitonin Gene-Related Peptide ...
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 D10.251 ... alpha-linolenic acid MeSH D10.251.355.450.450 - gamma-linolenic acid MeSH D10.251.355.840 - sorbic acid MeSH D10.251.355.920 - ... alpha-linolenic acid MeSH D10.251.355.310.640.425 - gamma-linolenic acid MeSH D10.251.355.325 - fatty acids, monounsaturated ...
6. Kemmann E, Ghazi D, Corsan G et al: Does ovulation stimulation improve fertility in women with minimal/mild endometriosis ... Drake TS, OBrien WF, Ramwell PW et al: Peritoneal fluid thromboxane B2 and 6-keto-prostaglandin F1 alpha in endometriosis. Am ... Buttram VC Jr, Reiter RC, Ward S: Treatment of endometriosis with danazol: report of a 6-year prospective study. Fertil Steril ... The cycle pregnancy rates were significantly lower in baboons with stage III-IV endometriosis (9%, 6/64) and with stage II ...
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 ...
... alpha as well as the urinary excretion of sodium and potassium. ... metabolite 6-keto-PGF1alpha [ Time Frame: Day 1 and Day 7 ]. * ...
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 ...
1). A 24-h urine collection on day 6 was used to evaluate dietary adherence through the determination of urinary sodium and ... Taken together with our previous RAS blockade studies (2,6), this hemodynamic response indicates that COX2 is an additional ... Daniel VC, Minton TA, Brown NJ, Nadeau JH, Morrow JD: Simplified assay for the quantification of 2,3-dinor-6-keto-prostaglandin ... F1 alpha by gas chromatography-mass spectrometry. J Chromatogr B Biomed Appl653 :117 -122,1994. ...
... 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 ... 6), and are exposed to portal vein concentrations of aspirin constantly, whereas circulating platelets are in the portal ... Figure 6. Aspirin concentration in the different circulation compartments. Aspirin concentration is represented by the density ... Simplified assay for the quantification of 2,3-dinor-6-keto-prostaglandin F1 alpha by gas chromatography-mass spectrometry. J ...
Here are the 6 doxycycline side effects you should be aware of. Find patient medical information for Ondansetron Hcl Oral on ... 300 mg, 400 mg, 600 mg, or 800 mg taken orally once every 6-8 hours; not to exceed 3200 mg/day. Monitor for GI risks. Dosage ... 1. Conjugated Linoleic Acid (CLA). This is a modified version of Omega-6 and not something your body can produce, so you have ... Labetalol had no effect on prostacyclin or thromboxane A2 as measured by urinary 6-keto-prostaglandin F1 alpha and serum ...
Limb vascular resistance (blood flow measured by venous occlusion plethysmography), prostaglandin I2 (as 6-ketoprostaglandin F1 ... alpha) and prostaglandin E2 plasma levels (detected by radioimmunoassay), and plasma catecholamines (detected by high- ... This increase was associated with a progressive decrease in cold-induced elevation of 6-ketoprostaglandin F1 alpha and ... p less than 0.05 for 6-ketoprostaglandin F1 alpha), whereas no significant correlations were found between variations of ...
Urinary excretion of dinor-thromboxane B2 and dinor-6-keto-prostaglandin F1 alpha was increased when the persistent pulmonary ... serial gas chromatographic mass spectrometric determination of their urinary metabolites dinor-thromboxane B2 and dinor-6-keto-prostaglandin ... F1 alpha, respectively. The patients were studied until their hypertension had resolved on clinical criteria. ...
  • Prostacyclin, which has a half-life of 42 seconds, [5] is broken down into 6-keto-PGF 1 , which is a much weaker vasodilator. (wikipedia.org)
  • Excretion of 2,3-dinor-6-keto-PGF1 alpha (reflecting prostacyclin generation) was not significantly influenced by any treatment. (nih.gov)
  • The endogenous biosynthetic capacity of the isolated cerebral capillary fractions for prostacyclin, measured as its chemically stable breakdown product, 6-keto-prostaglandin F1 alpha, was 11 ng/mg protein/10 min. (nih.gov)
  • The prostacyclin-synthesizing enzyme of the cerebral capillaries also converted the exogenously added prostaglandin endoperoxides to 6-keto-prostaglandin F1 alpha. (nih.gov)
  • We determined 6-keto prostaglandin F1 alpha since it is the stable metabolite of the bioactive prostacyclin. (asm.org)
  • Endogenous formation of thromboxane A2 and prostacyclin were evaluated in seven neonatates with persistent pulmonary hypertension by serial gas chromatographic mass spectrometric determination of their urinary metabolites dinor-thromboxane B2 and dinor-6-keto-prostaglandin F1 alpha, respectively. (bmj.com)
  • Based on their analysis on TLC, the COX products formed were identified as prostaglandins - PGF2alpha and prostacyclin derivative 6-keto PGF1alpha. (bvsalud.org)
  • Peripheral plasma levels of immunoreactive 6-oxo-PGF1 alpha, the stable hydrolysis product of prostacyclin, were significantly higher in female patients with tumours of the genital tract than in normal controls. (elsevier.com)
  • Identification of the major metabolite of prostacyclin and 6-ketoprostaglandin F1 alpha in man. (termsreign.cf)
  • 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. (jccm.es)
  • We investigated the effects of neuropeptide Y on the prostacyclin production of cultured porcine aortic endothelial cells by measuring the stable metabolite of prostacyclin, 6-keto-prostaglandin F1 alpha, by radioimmunoassay. (viisionsoliibrary19.gq)
  • Cigarette smoking increased the urinary excretion of 11-dehydro-thromboxane B2 (reflecting thromboxane A2 generation) and increased plasma concentration of the platelet alpha-granule constituents, platelet factor 4 and beta-thromboglobulin, compared with placebo treatment, indicating in vivo platelet activation. (nih.gov)
  • 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)
  • Then the amount of 6-keto PF1 alpha, thromboxane B2 and (TXB2) and PGE2 were serially measured both before and after hepatic resection. (biomedsearch.com)
  • 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. (ahajournals.org)
  • 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. (ahajournals.org)
  • 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 +/- 5% (mean +/- SD), respectively. (ahajournals.org)
  • We simultaneously determined the rate of release of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) into the suffusate. (ahajournals.org)
  • Urinary excretion of dinor-thromboxane B2 and dinor-6-keto-prostaglandin F1 alpha was increased when the persistent pulmonary hypertension was associated with group B streptococcal (n = 2) and pneumococcal (n = 1) sepsis. (bmj.com)
  • Concurrently, the urinary excretions of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha(6-keto-PGF1 alpha) decreased gradually in parallel with the renal function parameters, whereas the urinary excretion of thromboxane B2 (TXB2) increased markedly. (semanticscholar.org)
  • After injury+/-subcutaneous diclofenac pretreatment, we investigated the behavioural response (changes to thermally-induced tail flick latency) and measured diclofenac, prostaglandin E(2), 6-keto-prostaglandin F(1 alpha) and thromboxane B(2) concentrations in the tail, spinal cord and brain. (nih.gov)
  • thromboxane B2 nd 6-ketoprostaglandin F1.alpha. (geoscience.net)
  • Lung function and plasma levels of thromboxane B2, 6-ketoprostaglandin F1 alpha and beta-thromboglobulin in antigen-induced asthma before and after indomethacin pretreatment. (openaire.eu)
  • Plasma phospholipase A2 (PLA2) activity, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TXB2) levels were measured at various times during cardiac surgery. (mysciencework.com)
  • Changes in plasma prostaglandin F2, thromboxane B2 and 6-keto-prostaglandin F1 alpha contents in patients suffering from multiple system organ failure after burns From nucleotide sequence analysis, qacA is predicted to encode a protein of Mr 55017 containing 514 amino acids. (courtfield.ml)
  • Choroid plexus and intact surface vessels synthesized 6-keto-prostaglandin F1 alpha at 37 and 35 ng/mg protein/10 min, respectively. (nih.gov)
  • Comparison of the synthesis of prostaglandins 6-keto-F1 alpha, E2, and F2 alpha showed that 6-keto-prostaglandin F1 alpha was the major prostaglandin formed in the microvessels, in the larger surface vessels, and in the choroid plexus. (nih.gov)
  • The increase of vascular resistance was significantly correlated with the decrease of both prostaglandins (r = 0.93, p less than 0.05 for prostaglandin E2 and r = 0.89, p less than 0.05 for 6-ketoprostaglandin F1 alpha), whereas no significant correlations were found between variations of vascular resistance and catecholamines. (ahajournals.org)
  • Soil persistence and metabolism of N-sec-butyl-4-tert-butyl-2,6-dinitroaniline. (courtfield.ml)
  • Secondary objectives are the characterization of the urinary excretion of prostaglandin E2 (PGE2) and the prostaglandin I2 (PGI2) metabolite 6-keto-prostaglandin F1 (PGF1)alpha as well as the urinary excretion of sodium and potassium. (clinicaltrials.gov)
  • Verapamil decreased the baseline values of 6-keto-PGF1 alpha and increased those of TXB2. (ahajournals.org)
  • Verapamil inhibited the ischemia-reperfusion-induced increase in 6-keto-PGF1 alpha but did not alter the effect of ischemia-reperfusion on TXB2. (ahajournals.org)
  • In patients who did not respond to treatment or with tumour recurrence, levels of plasma 6-oxo-PGF1 alpha remained high or even rose further. (elsevier.com)
  • Benign gynaecological tumours were also associated with significantly raised plasma 6-oxo-PGF1 alpha levels, and these fell to normal levels immediately on surgical removal of the tumour. (elsevier.com)
  • Further investigations are warranted to see whether serial measurements of plasma 6-oxo-PGF1 alpha could be used as a prognostic index for the clinical status of patients with gynaecological tumours. (elsevier.com)
  • This was highly correlated with concurrent increases in plasma 6-keto-PGF1 alpha, TXB2 concentrations did not increase with heparin administration but did increase significantly after initiation of CPB. (mysciencework.com)
  • High plasma PLA2 activity, 6-keto-PGF1 alpha, and TXB2 concentrations were measured throughout the CPB period. (mysciencework.com)
  • Protamine, administered to neutralize the heparin, caused an acute reduction of both plasma PLA2 activity and plasma 6-keto-PGF1 alpha, but no change in plasma TXB2 concentrations. (mysciencework.com)
  • Thus the ratio of TXB2 to 6-keto-PGF1 alpha increased significantly after protamine administration. (mysciencework.com)
  • In conclusion, plasma PLA2 activity and 6-keto-PGF1 alpha concentrations are markedly enhanced with systemic heparinization. (mysciencework.com)
  • In addition the pulmonary vasoconstriction sometimes associated with protamine infusion during cardiac surgery might be due to decreased plasma PLA2 activity, with an associated increased TXB2/6-keto-PGF1 alpha ratio. (mysciencework.com)
  • Levels of urinary 6-keto-PGF1-alpha (pg/ml) were measured by specific radioimmunoassay. (jccm.es)
  • PGI2 is derived from the ω-6 arachidonic acid. (wikipedia.org)
  • Renal tissue levels of CGRP and 6-keto-prostaglandin F1alpha, a stable metabolite of PGI2, increased after renal ischemia/reperfusion, peaking at 1 h after reperfusion. (unboundmedicine.com)
  • Pretreatment with capsazepine, CGRP(8-37), indomethacin, and denervation of primary sensory nerves significantly increased blood urea nitrogen and serum creatinine levels, renal vascular permeability, renal tissue levels of myeloperoxidase activity, cytokine-induced neutrophil chemoattractant, and tumor necrosis factor-alpha, and decreased renal tissue blood flow. (unboundmedicine.com)
  • 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)
  • This study shows that MDHM-activated macrophages not only released interleukin-6 (IL-6) but also exhibited increased synthesis of cell-associated IL-1 as well as liberation of tumor necrosis factor and prostaglandin. (asm.org)
  • Limb vascular resistance (blood flow measured by venous occlusion plethysmography), prostaglandin I2 (as 6-ketoprostaglandin F1 alpha) and prostaglandin E2 plasma levels (detected by radioimmunoassay), and plasma catecholamines (detected by high-performance liquid chromatography and electrochemical detection) were measured. (ahajournals.org)
  • Prostaglandin E2, prostaglandin F2 alpha, and 6-keto prostaglandin F1 alpha concentrations of gastric mucosal biopsy specimens, obtained endoscopically, were measured by radioimmunoassay. (redfernstrategic.com)
  • In the control group, both 6-keto PF1 alpha and PGE2 showed only a slight increase both during and after the operation. (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)
  • Increases in renal tissue levels of 6-keto-prostaglandin F1alpha at 1 h after reperfusion were significantly inhibited by pretreatment with capsazepine, CGRP(8-37), and indomethacin. (unboundmedicine.com)
  • Because blockade of the renin angiotensin system (RAS) does not completely normalize hyperfiltration ( 6 ), it is clear that other factors are operative in the renal microcirculation in diabetes. (diabetesjournals.org)
  • However, despite improved understanding, the prognosis of HRS remained poor, and in the 1970s, the term "terminal functional renal failure" was synonymous with HRS ( 6 ). (asnjournals.org)
  • 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)
  • Suppression of plasma 6-keto-prostaglandin F1 alpha and 13,14-dihydro-15-keto-prostaglandin F2 alpha by aminoglutethimide in advanced breast cancer. (ox.ac.uk)
  • There are various ways to form Prostaglandin F2 alpha ( PGF2 alpha ). (bio-rad.com)
  • 12-Hydroxyheptadecatrienoic acid (HHT), prostaglandin F2.alpha. (geoscience.net)
  • 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)
  • 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)
  • 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)
  • Further, CP-1158 attenuated LPS-induced syntheses of tumor necrosis factor (TNF)-alpha, IL-1beta, interferon-inducible protein (IP)-10 and macrophage inflammatory protein (MIP)-1beta transcripts. (termsreign.cf)
  • 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)
  • This increase was associated with a progressive decrease in cold-induced elevation of 6-ketoprostaglandin F1 alpha and prostaglandin E2 plasma levels until, after five stimulations, neither prostaglandin was detectable. (ahajournals.org)
  • 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)
  • Both observational studies ( 1-5 ) and controlled clinical trials ( 6 ) support the concept that aspirin prevents mortality and metastasis from adenocarcinomas. (aacrjournals.org)
  • Overview of the clinical development and results of a quadrivalent HPV (types 6, 11, 16, 18) vaccine. (redfernstrategic.com)
  • 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)
  • Overexpression of platelet-type 12-lipoxygenase promotes tumor cell survival by enhancing alpha(v)beta(3) and alpha(v)beta(5) integrin expression. (tcd.ie)
  • After inducing pulmonary hypertension through a single subcutaneous injection of MCT (60 mg/kg) to Sprague-Dawley rats, we administered daily intraperitoneal injections of either glycyrrhizin (GLY, 50 mg/kg), an inhibitor of HMGB1, or saline (control) for either 4 or 6 weeks. (termsreign.ml)
  • One hour after LPS injection, a significant mean increase of TNF-alpha in mouse serum was observed. (neuekrebstherapie-kleintierpraxis.de)
  • 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)
  • MDHM, a macrophage-stimulatory product of Mycoplasma fermentans, leads to in vitro interleukin-1 (IL-1), IL-6, tumor necrosis factor, and prostaglandin production and is pyrogenic in rabbits. (asm.org)
  • Glucose 1,6-bisphosphate and the mechanism of the Pasteur effect in diaphragm muscle. (docphin.com)
  • Are we missing a good definition for 6-aminonicotinamide ? (definitions.net)
  • Priming with gamma interferon further increased MDHM-mediated IL-6 release. (asm.org)
  • The property of MDHM to cause IL-6 release from macrophages and the IL-6 growth dependency of the 7TD1 hybridoma cell line were made use of in a coculture assay system to quantitate the activity of MDHM. (asm.org)