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Biomedical subjects

M Laposata

Publications and source records attributed to M Laposata.

At least 19 recordsLinked to original sources
PubMed1996

Fatty acid ethyl esters in the blood as markers for ethanol intake.

OBJECTIVE: To determine the clinical utility of fatty acid ethyl esters (FAEEs) in the blood as a short-term confirmatory marker for ethanol intake and a longer-term marker for ethanol intake after ethanol is no longer detectable. DESIGN: Single-center controlled clinical trial and a blinded comparison involving 48 blood samples that were positive, negative, or equivocal for blood ethanol. PARTICIPANTS: Seven healthy subjects (4 men and 3 women, aged 21 to 23 years) participated in the clinical trial. Blood samples from participants for the blinded comparison portion of the study were numbered from 1 to 48 and not identified by name. INTERVENTION: The 7 healthy subjects ingested a known amount of ethanol at a fixed rate. The concentration of FAEEs in the blood after ethanol intake was determined for a period of up to 24 hours. There was no intervention in the blinded comparison study. MAIN OUTCOME MEASURES: In the clinical trial, a pharmacokinetic analysis of FAEE concentration in the blood after ethanol intake was completed for 7 individuals whose blood ethanol level was elevated from 25 to 35 mmol/L. In the blinded comparison, the 48 blood samples that were positive, negative, or equivocal for blood ethanol were analyzed for FAEE concentration. RESULTS: In the clinical trial, the disappearance of FAEEs from the blood followed a decay curve that initially resembled the decay curve for blood ethanol. However, because of a very slow secondary elimination phase, the FAEEs were found to persist in the blood for at least 24 hours after ethanol intake was completed. In the blinded comparison, all 20 samples that were positive for ethanol were positive for FAEEs, 7 of 7 samples equivocal for ethanol were positive for FAEEs, and 21 of 21 negative samples for ethanol were negative for FAEEs. CONCLUSIONS: Serum concentration of FAEEs can serve as an excellent short-term confirmatory test for ethanol intake as well as a longer-term marker of ethanol ingestion. Measurement of FAEEs in the blood may be a more sensitive indicator of ethanol ingestion than the measurement of blood ethanol .

Adult↗
PubMed1996

Purification of fatty acid ethyl esters by solid-phase extraction and high-performance liquid chromatography.

We have developed a two-step method to purify fatty acid ethyl esters (FAEE) using solid-phase extraction (SPE), with a recovery of 70 +/- 3% (mean +/- S.E.M.) as assessed using ethyl oleate as a recovery marker from a standard lipid mixture in hexane. The first step of the SPE procedure involves application of a lipid mixture to an aminopropyl-silica column with simultaneous elution of FAEE and cholesteryl esters from the column with hexane. Gas chromatographic analysis of FAEE without interference from cholesteryl esters may be performed using the eluate from the aminopropyl-silica column, thus eliminating the need for an octadecylsilyl (ODS) column in this case. The FAEE can then be separated from the cholesteryl esters, if necessary, by chromatography on an ODS column and elution with isopropanol-water (5:1, v/v). Both the aminopropyl-silica and ODS columns were found to be effective for up to four uses. To permit isolation of specific FAEE species following isolation of total FAEE by the two-step SPE method, we have also developed a purification scheme for individual FAEE by high-performance liquid chromatography (HPLC). Thus, this simple method allows for reproducible isolation of total FAEE by SPE and isolation of individual FAEE species by HPLC.

Chromatography, High Pressure Liquid↗
PubMed1996

gamma-Linolenic acid treatment of rheumatoid arthritis. A randomized, placebo-controlled trial.

OBJECTIVE: To assess the clinical efficacy and adverse effects of gamma-linolenic acid (GLA), a plant seed oil-derived unsaturated fatty acid that suppresses inflammation and joint tissue injury in animal models, in the treatment of active rheumatoid arthritis (RA). METHODS: Fifty-six patients with active RA were randomized to treatment groups in a 6-month, double-blind trial of GLA versus placebo. This was followed by a 6-month, single-blind trial during which all patients received GLA. Patients were treated with 2.8 gm/day of GLA as the free fatty acid or with sunflower seed oil (placebo) administered in identical capsules. RESULTS: Treatment with GLA for 6 months resulted in statistically significant and clinically relevant reductions in the signs and symptoms of disease activity in patients with RA. Overall meaningful responses (at least 25% improvement in 4 measures) were also better in the GLA treatment group (14 of 22 patients versus 4 of 19 in the placebo group; P = 0.015). During the second 6 months, both groups exhibited improvement in disease activity. Thus, patients taking GLA during the entire study showed progressive improvement during the second 6 months. In this group, 16 of 21 patients showed meaningful improvement at 12 months compared with study entry. CONCLUSION: GLA at doses used in this study is a well-tolerated and effective treatment for active RA. GLA is available as a component of several plant seed oils and is usually taken in far lower doses than were used in this trial. It is not approved in the United States for the treatment of any condition, and should not be viewed as therapy for any disease. Further controlled studies of its in RA are warranted.

Adolescent↗
PubMed1996

Thioesterification of platelet proteins with saturated and polyunsaturated fatty acids.

We have demonstrated that more than 20 platelet proteins can be acylated with fatty acids via thioester linkages. These include the glycoprotein IX beta chain of glycoprotein Ib, components of the von Willebrand factor receptor on the platelet surface, P-selectin, and alpha subunits of Gz, Gq, and Gi. Our studies have shown that platelet proteins can be posttranslationally acylated in thioester linkages not only with palmitate but with myristate and also with the eicosanoid precursor fatty acids arachidonate and eicosapentaenoate. Thioesterification of platelet proteins with fatty acids other than palmitate may have significant functional consequences for reversible binding of proteins to membranes.

Arachidonic Acid↗
PubMed1996

Coagulation changes during thoracoabdominal aneurysm repair.

PURPOSE: The cause of coagulopathic hemorrhage during thoracoabdominal aneurysm (TAA) repair has not been well defined in human studies. We investigated changes in the coagulation system associated with supraceliac versus infrarenal cross-clamping to address this critical issue. METHODS: Blood levels of fibrinogen, the prothrombin fragment F1.2, D-dimer, and factors II, V, VII, VIII, IX, X, XI, and XII were analyzed in 19 patients with TAAs and four patients with abdominal aortic aneurysms (AAAs) at: (A) induction; (B) 30 minutes into supraceliac (TAA) or infrarenal (AAA) clamping; (C) 30 minutes after release of supraceliac or infrarenal clamps; and (D) immediately after surgery. Preoperative and intraoperative variables, including but not limited to aneurysm type, pathologic findings, comorbid conditions, clamp times, volume and timing of blood products, and clinical outcome, were prospectively recorded. Significance was determined by analysis of variance, Student's t test, and univariate linear regression. RESULTS: Levels of fibrinogen and factors II, V, VIII, VIII, IX, X, XI, and XII decreased (p < 0.05) at time B versus time A and returned to near baseline by time D. D-dimer and F1.2 increased starting at time B and reached significance (p < 0.05) by time D. Data points were compared for the TAA and AAA groups. Although AAA groups demonstrated a trend to factor activity reduction and increased fibrinolysis, the effect was much less pronounced than in TAA and did not approach significance. No correlation of coagulation change with clamping time was present; however, visceral clamping times were all less than 65 minutes (mean, 44 minutes). Blood and factor replacement was initiated after time B. Univariate regression analysis of factor level versus total blood replacement demonstrated a significant (p < 0.04) correlation between the reduction in the levels of factors II, V, VII, VIII, X, and XII, and the increase in the level of D-dimer at time B and subsequent total blood replacement. CONCLUSIONS: Thoracoabdominal aneurysm repair is associated with a reduction in clotting factor activity and an increase in fibrinolytic function, which occurs after placement of the supraceliac clamp. Explanations include visceral ischemia or a greater and longer ischemic tissue burden as the likely cause of coagulation alterations. Total blood replacement during TAA procedures was correlated to the degree of factor reduction and fibrinolysis at the time of visceral cross-clamping. An aggressive approach to early blood component replacement and to coagulation monitoring could lessen blood loss during TAA repair and avoid potentially disastrous bleeding complications.

Aortic Aneurysm, Abdominal↗
PubMed1996

What many of us are doing or should be doing in clinical pathology: a list of the activities of the pathologist in the clinical laboratory.

Mr. Paul Mango, Chief Operating Officer of a hospital-based clinical laboratory network in Pittsburgh, recently performed a survey of patients presenting for phlebotomy. The survey included the question, "What does a pathologist do?" The results were that 50% of the patients had no idea what a pathologist did, and 30% of the patients stated that pathologists examined dead bodies. It is not surprising that there is a limited understanding by patients of the activities of pathologists because patients do not usually see pathologists. However, beyond autopsy and surgical pathology, the activities of pathologists are also not well known to nonpathologist physicians and hospital administrators. A poor understanding of activities in clinical pathology have placed these clinical responsibilities of the pathologist under particular scrutiny for cost reduction. The quantitation of output from anatomic pathology, in number of slides reviewed or number of autopsies performed, is objective and easily understood. As noted in the list of clinical pathology activities that follows, the responsibilities within the clinical laboratory are highly diverse and, if the pathologist handles them successfully, highly contributory to patient care. Thus, it is timely that a compilation of activities in clinical pathology be issued for review by the pathologist community. I would hope that this list will serve as a starting point for a universally accepted group of activities that describes clinical pathology today and that it will be useful for pathologists to make their significant contributions in the clinical laboratory apparent to administrators, fellow physicians, and patients. The clinical laboratory responsibilities should also be valuable to directors of residency training programs to focus training in clinical pathology toward the development of currently desirable expertise.

Clinical Laboratory Techniques↗
PubMed1996

Reduced fatty acid ethyl ester synthase activity in the white blood cells of alcoholics.

PURPOSE: Fatty acid ethyl esters (FAEEs), esterification products of ethanol and fatty acids, have been implicated as mediators of ethanol-induced organ damage. It has been shown that FAEE synthase, the enzyme responsible for the formation of FAEE, is present selectively in the organs commonly damaged by ethanol abuse. Recently, we have made the observation that FAEEs are also present in the serum after ethanol ingestion. The current study was performed to determine whether cellular elements of the blood and/or plasma are capable of synthesizing FAEEs from fatty acids and ethanol. MATERIALS AND METHODS: Heparinized blood samples were collected from 10 healthy volunteers, and the red blood cells, platelets, plasma, and several white blood cell populations were assayed for FAEE synthase activity. Blood samples from control subjects and individuals admitted to an alcoholic detoxification unit at a local hospital were also assayed for FAEE synthase activity. RESULTS: We observed that the FAEE synthase activity is present in whole blood, primarily within white blood cells. Fractionation of the white blood cells revealed that the lymphocyte-monocyte fraction isolated using Ficoll-hypaque contained approximately 3.5-fold higher activity than the granulocyte fraction. The cell type that contained the highest FAEE synthase activity (1220 pmol/hr/10(6) cells) was the natural killer (NK) cell population. B cells contained approximately 40% of the enzyme activity found in NK cells, and the B-cell activity was slightly greater than that found in CD4+ and CD8+ T cells. Having shown that FAEE synthase exists in a blood cell, we subsequently demonstrated that alcoholic individuals have approximately half the white blood cell FAEE synthase activity of that found in normal controls. We also demonstrated that white blood cell FAEE synthase could be induced nearly 2-fold upon ingestion of 2 oz of scotch whiskey for 6 days. The enzyme activity returned to baseline levels despite ingestion of 2 oz of scotch whiskey/day for 3 additional days. CONCLUSIONS: These data indicate that ethanol ingestion results in increased FAEE production, particularly by NK cells. FAEE synthesis after ethanol ingestion may explain the presence of FAEE in the serum. The lower enzyme activity observed in white blood cells of alcoholics from a detoxification center may be the result of years of ethanol abuse or it may be that alcoholics congenitally have low levels of FAEE synthase. If the latter is true, this finding may explain in part the genetic predisposition of many alcoholic individuals to ethanol abuse.

Acyltransferases↗
PubMed1996

Fatty acid ethyl ester synthase, an enzyme for nonoxidative ethanol metabolism, is present in serum after liver and pancreatic injury.

Fatty acid ethyl esters (FAEE), esterification products of ethanol and fatty acids, have been implicated as mediators of ethanol-induced organ damage. Because cytosolic enzymes such as aspartate aminotransferase, lipase, and amylase appear in the blood after liver or pancreatic damage, we hypothesized that FAEE synthase, which is both cytosolic and membrane bound, is also released into the blood of patients with liver or pancreatic disease. We used a method involving thin-layer chromatography coupled with gas chromatography-mass spectrometry to reliably identify and quantify FAEE. In this study, we demonstrated that patients with liver or pancreatic disease release FAEE synthase into their plasma in amounts proportional to the amount of aspartate aminotransferase (r = 0.78), amylase (r = 0.65), and lipase (r = 0.63). These data indicate that liver and pancreatic damage results in release of FAEE synthase into the blood. The presence of FAEE synthase in plasma permits nonoxidative ethanol metabolism in the plasma.

Acyltransferases↗
PubMed1996

Binding of ethyl oleate to low density lipoprotein, phospholipid vesicles, and albumin: a 13C NMR study.

Fatty acid ethyl esters (FAEE), esterification products of ethanol and fatty acids, have been implicated as mediators of ethanol-induced organ damage. After ethanol ingestion in humans, FAEE circulate in blood, bound to lipoproteins and albumin. We have analyzed the binding of ethyl (1-13C, 99%) oleate (EO) to small unilamellar phospholipid vesicles (SUV), human low density lipoprotein (LDL), and bovine serum albumin (BSA) by 13C-NMR spectroscopy. Binding of < or = 25 mol% EO to SUV yielded a single EO carbonyl peak (172.6-172.9 ppm) downfield from that of EO oil (171.9 ppm). Thus, the carbonyl forms hydrogen bonds with water in the SUV aqueous interface. At 30 mol% EO in SUV, a second EO carbonyl peak appeared, indicating a limit in FAEE solubility in SUV. Addition of EO to isolated human LDL yielded a peak at 171.9 ppm, suggesting that the EO exists in an unhydrated environment, most likely the core of the lipoprotein. This binding was also observed using high levels of EO added to human serum. The addition of EO dissolved in ethanol or as an oil to a solution of BSA yielded no visible EO peak, whereas addition of (1-13C, 99%) oleic acid resulted in several narrow peaks, demonstrating a much greater affinity of BSA for oleic acid than for EO. Bidirectional transfer of EO between LDL and SUV was observed and was 85% complete within 30 min. There was no measurable transfer of EO from LDL or SUV to albumin. The weak binding of EO to albumin will result in increased transport of EO by lipoproteins as plasma levels of EO increase.

Carbon Isotopes↗
PubMed1995

Fatty acid ethyl ester synthase catalyzes the esterification of ethanol to cocaine.

Fatty acid ethyl esters (FAEE), esterification products of ethanol and fatty acids, have been implicated as mediators of ethanol induced organ damage. It has been shown that FAEE synthase, the enzyme responsible for the formation of FAEE, is present selectively in the organs damaged by ethanol abuse. Cocaethylene is a cocaine metabolite generated in the presence of ethanol which has been established as enhancing cocaine toxicity. In the present study we show that purified FAEE synthase also catalyzes the formation of cocaethylene. A linear relationship (r = 0.998) was demonstrated between the amount of purified FAEE synthase (microgram) and cocaethylene synthesis (nmol/hr). We further showed a correlation (r = 0.804) between the two enzyme activities in selected tissues. These findings provide evidence that purified FAEE synthase has cocaethylene synthetic ability and FAEE synthase may be responsible for a portion of cocaethylene synthesis in vivo.

Acyltransferases↗
PubMed1995

Differential regulation of human T lymphocyte protein kinase C activity by unsaturated fatty acids.

Administration of gamma-linolenic acid suppresses active synovitis in patients with rheumatoid arthritis. We therefore examined the effects of gamma-linolenic acid and its first metabolite, dihomo-gamma-linolenic acid, on protein kinase C, a key element in transduction of signals from cell surface to nucleus. We report here that gamma-linolenic acid and dihomo-gamma-linolenic acid suppress total protein kinase C activity, but facilitate translocation of protein kinase C activity from cytosol to membrane in human peripheral blood T lymphocytes stimulated with phorbol 12-myristate 13-acetate. Arachidonic acid and eicosapentaenoic acid do not influence total protein kinase C activity and have only modest effects on enzyme translocation. These findings in whole cells are in contrast to results of experiments performed with isolated protein kinase C, in which unsaturated fatty acids uniformly enhance protein kinase C activity. The differential effects of unsaturated fatty acids underscore the complexity of protein kinase C regulation and indicate that gamma-linolenic and dihomo-gamma-linolenic acids influence T lymphocyte protein kinase C metabolism in a manner that is unique among unsaturated fatty acid precursors of eicosanoids.

8,11,14-Eicosatrienoic Acid↗
PubMed1995

Fatty acid ethyl esters decrease human hepatoblastoma cell proliferation and protein synthesis.

BACKGROUND/AIMS: Fatty acid ethyl esters (FAEEs) are nonoxidative products of ethanol metabolism. They have been implicated as mediators of ethanol-induced organ damage because FAEE and FAEE synthase have been found specifically in the organs damaged by ethanol abuse. This study showed toxicity specifically related to FAEE or their metabolites for intact human hepatoblastoma-derived cells (HepG2). METHODS: The lipid core of human low-density lipoprotein (LDL) was extracted and the LDL particle reconstituted with either ethyl oleate or ethyl arachidonate. Cultured HepG2 cells were incubated with LDL containing FAEE. Cell proliferation was measured by [methyl-3H]thymidine incorporation. Protein synthesis was determined using L-[35S]methionine. RESULTS: Incubation of cells with 600 mumol/L ethyl oleate or 800 mumol/L ethyl arachidonate decreased [methyl-3H]thymidine incorporation into HepG2 cells by 31% and 37%, respectively. LDL reconstituted with 400 mumol/L ethyl oleate decreased protein synthesis in intact HepG2 cells by 41%. Electron microscopy revealed significant changes in cell morphology, particularly involving the cell nucleus. FAEE delivered in reconstituted LDL were rapidly hydrolyzed and the fatty acids re-esterified into phospholipids, triglycerides, and cholesterol esters, with preference for triglycerides. CONCLUSIONS: These findings provide evidence that FAEE are toxic for intact human hepatoblastoma cells and that they or their metabolites may be an important causative agent in ethanol-induced liver damage.

Cell Division↗
PubMed1995

Fatty acids. Biochemistry to clinical significance.

Fatty acids are a major source of lipids in the diet. Dietary fatty acids are able to significantly influence the concentration of serum cholesterol and thereby influence the risk of atherosclerosis. This brief review on fatty acids will present information on the structure and nomenclature of fatty acids, the metabolic pathways for fatty acids in cells, and the influence of dietary fatty acids on serum cholesterol levels.

Cholesterol↗
PubMed1995

Low-density lipoprotein reconstituted with fatty acid ethyl esters as a physiological vehicle for ethyl ester delivery to intact cells.

Fatty acid ethyl esters (FAEEs), esterification products of ethanol and fatty acids, have been found selectively in the organs damaged by ethanol abuse, and on that basis have been implicated as contributors to ethanol-induced organ damage. To directly assess the cytotoxic potential of FAEEs with intact cells in a physiological system, solubility must be achieved for these highly nonpolar lipids in aqueous medium. After ethanol ingestion, FAEEs can be found within low-density lipoproteins (LDLs). Therefore, to achieve solubility with FAEEs bound to a naturally occurring lipid carrier, we developed a method for FAEE solubilization and delivery to cells in culture. We synthesized radiolabeled FAEEs and incorporated them into human LDL particles that bind to LDL receptors and deliver FAEEs to intact cells. Ethyl palmitate and ethyl oleate were incorporated into LDLs yielding molar ratios of FAEEs to LDLs of 2,153 +/- 249 and 4,208 +/- 403, respectively. LDL reconstituted with FAEE had the same electrophoretic mobility on agarose gel electrophoresis as native LDL, indicating that the reconstituted LDL (rLDL) was not oxidatively modified. Quantitative analysis of the solubilization of FAEEs in aqueous medium was investigated by adding FAEEs to tissue culture medium either directly or reconstituted in LDL at a concentration of 27 microM. The percentage of FAEE quantitated was 40.0 +/- 2.5% and 89.3 +/- 0.6% for FAEEs added directly and in rLDLs, respectively. After sterile filtration of these two media, the percentage of FAEE that remained was 11.8 +/- 1.3% (direct addition) and 74.9 +/- 1.3% (addition within rLDL), further demonstrating that the LDL particle did solubilize the FAEE.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoma, Hepatocellular↗
PubMed1995

Near patient blood glucose monitoring.

This report describes the quality control and quality assurance programs for bedside glucometry at our institution. From our 3-year experience, a regular schedule of inspections is necessary for maintenance of high-quality bedside glucose testing. The most common violation of quality control/quality assurance in bedside glucometry in our institution was the failure to perform regular proficiency testing, in which one random patient's bedside capillary blood glucose value during each inspection period was compared to his or her venous plasma or serum glucose value obtained from the central laboratory. Failure to perform instrument maintenance and document operator certification were the next most common violations of quality control/quality assurance in our bedside glucometry program. Regarding the cost analysis for bedside glucometry, we conclude that bedside glucose testing is not inherently more expensive than testing performed within the clinical laboratory. The increased cost of bedside glucometry over laboratory testing can be significantly minimized by involvement of a limited number of health care workers and performance of bedside glucometry only on clinical units where testing is required more than five times per day.

Blood Glucose↗
PubMed1995

Mode of transport of fatty acid to endothelial cells influences intracellular fatty acid metabolism.

Fatty acids are transported to cells from a variety of different moieties in the plasma. In this study, using oleate and human umbilical vein endothelial cells, we asked whether the vehicle that delivers fatty acid to cells has an influence on its metabolism upon its incorporation into the cell. For oleate vehicles, we compared free oleate bound to albumin with oleate in low density lipoprotein (LDL) which was delipidated and reconstituted with either radiolabeled triolein or cholesteryl oleate. Using approximately physiologic concentrations of LDL and free oleate, we demonstrated by three lines of evidence unique patterns of cellular oleate metabolism for oleate delivered as triolein within LDL, for oleate delivered as cholesteryl oleate within LDL, and for oleate delivered as free oleate bound to albumin. In fact, the difference was most marked between cholesteryl oleate and triolein, even though the oleate in cholesteryl oleate and triolein was delivered in identically reconstituted LDL particles, which were presumably incorporated into the cells and degraded in lysosomes in a similar fashion. First, we demonstrated that oleate delivered as free oleate or as triolein in reconstituted LDL was desaturated and elongated to fatty acid metabolites, but cholesteryl oleate in reconstituted LDL was not similarly metabolized. The elongated and desaturated metabolites of oleate were preferentially esterified in cellular triglyceride when oleate was delivered as free oleate, but they were preferentially esterified in phospholipids when oleate was delivered as triolein in LDL. Second, we observed that there was a difference in the distribution of oleate among phospholipids when oleate was delivered as cholesteryl oleate in reconstituted LDL versus triolein in reconstituted LDL. When the oleate was delivered as triolein in reconstituted LDL, there was greater esterification in diacyl phosphatidylethanolamine, in phosphatidylserine, and in phosphatidylinositol. When oleate was delivered as cholesteryl oleate in reconstituted LDL, there was greater esterification in diacyl phosphatidylcholine. Third, there was a marked preference for oleate delivered from triolein in LDL over cholesteryl oleate in LDL for esterification into the sn-1 position of plasmalogens as a vinyl ether-linked fatty acid. These data indicate that mode of transport of fatty acid to cells influences fatty acid metabolism upon its incorporation into the cell, even when the fatty acid is delivered from the core of the same lipoprotein.

Binding Sites↗
PubMed1994

Covalent binding of arachidonate to G protein alpha subunits of human platelets.

The alpha subunits of GTP-binding regulatory proteins (G proteins) are subject to lipid modifications required for anchorage to membrane and/or interactions with other proteins. With the knowledge that alpha subunits are palmitoylated, which we demonstrate here for human platelets, we sought to determine whether these subunits also bind arachidonate and myristate in a covalent, post-translational manner. All alpha subunits examined were found to incorporate radioactivity upon incubation of human platelets with [3H]palmitate, [3H]arachidonate, and [3H]myristate. The identity of [3H]palmitate and [3H]arachidonate as covalently bound fatty acids was confirmed by high pressure liquid chromatography following alkaline methanolysis. With [3H]myristate, however, the bound fatty acid proved to be [3H]palmitate, presumably generated by a 2-carbon chain elongation. Protein-bound [3H]palmitate and [3H]arachidonate were released by hydroxylamine at neutral pH, implying a thioester linkage between protein and fatty acid. Thus, post-translational modifications of G protein alpha subunits include palmitoylation and arachidonoylation, but not myristoylation. Given the different physical properties of saturated and unsaturated fatty acids and the large-scale release of arachidonate during platelet activation, changes in arachidonate incorporation may serve as an important regulator of alpha subunit function.

Alprostadil↗