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PubMedDate not supplied

Sodium nitroprusside-induced rat fundus relaxation is ryanodine-sensitive and involves L-type Ca2+ channel and small conductance Ca(2+)-sensitive K+ channel components.

1 The aim of this study was to examine whether sodium nitroprusside (SNP)-induced relaxation of rat fundus longitudinal smooth muscle involves ryanodine-sensitive Ca2+ release. 2 SNP (300 nM-30 microM) elicited concentration-dependent relaxation of precontracted (1 microM carbachol) rat fundus, an effect almost abolished by the selective guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one (ODQ, 10 microM). 3 SNP-mediated relaxations were almost abolished by 10 microM ryanodine. 4 SNP-mediated relaxations were also reduced by either 1 microM apamin (a selective small conductance Ca(2+)-sensitive K+ channel, SKCa, inhibitor) or the selective L-type Ca2+ channel inhibitor, nicardipine (3 microM). 5 SNP-induced relaxations were insensitive to 1 mM tetraethylammonium chloride (an inhibitor of large-conductance Ca(2+)-sensitive K+ channels) and 1 microM glibenclamide (an ATP-sensitive K+ channel inhibitor). 6 These data suggest that SNP-mediated fundus relaxation occurs via a cGMP-mediated and ryanodine-sensitive mechanism which requires, at least in part, SKCa and L-type Ca2+ channel activity.

Animals↗
PubMed2006

Acid-sensitive ionic channels in midbrain dopamine neurons are sensitive to ammonium, which may contribute to hyperammonemia damage.

Acid-sensitive ion channels (ASICs) are proton-gated and belong to the family of degenerin channels. In the mammalian nervous system, ASICs are most well known in sensory neurons, where they are involved in nociception, occurring when injury or inflammation causes acidification. ASICs also are widely expressed in the CNS, and some synaptic roles have been revealed. Because neuronal activity can produce pH changes, ASICs may respond to local acidic transients and alter the excitability of neuronal circuits more widely than is presently appreciated. Furthermore, ASICs have been found to underlie calcium transients that contribute to neuronal death. Degeneration of midbrain dopamine neurons is characteristic of advanced idiopathic Parkinson's disease. Therefore, we tested for functional ASICs in midbrain dopamine neurons of the ventral tegmental area and substantia nigra compacta. Patch-clamp electrophysiology applied to murine midbrain slices revealed abundant acid-sensitive channels. The ASICs were gated and desensitized by extracellular application of millimolar concentrations of NH(4)Cl. Although the NH(4)Cl solution contains micromolar concentrations of NH(3) at pH 7.4, our evidence indicates that NH(4)(+) gates the ASICs. The proton-gated and the ammonium-gated currents were inhibited by tarantula venom (psalmotoxin), which is specific for the ASIC1a subtype. The results show that acid-sensitive channels are expressed in midbrain dopamine neurons and suggest that ammonium sensitivity is a widely distributed ASIC characteristic in the CNS, including the hippocampus. The ammonium sensitivity suggests a role for ASIC1s in hepatic encephalopathy, cirrhosis, and other neuronal disorders that are associated with hyperammonemia.

Acid Sensing Ion Channels↗
PubMed1981

Substrate proteins for calmodulin-sensitive and phospholipid-sensitive Ca2+-dependent protein kinases in heart, and inhibition of their phosphorylation by palmitoylcarnitine.

At least two substrate proteins for phospholipid-sensitive Ca2+-dependent protein kinase and at least six substrates for calmodulin-sensitive Ca2+-dependent protein kinase were identified in the cytosol of the guinea pig heart. In the particulate subfractions enriched in nuclei, mitochondria, microsome, or plasma membrane, no substrates for the phospholipid-sensitive enzyme were demonstrated but at least four substrates for the calmodulin-sensitive enzyme were identified. The present studies suggest that phospholipid, acting independently of calmodulin, is likely to be involved in the regulation of Ca2+-dependent protein phosphorylation in the heart. Phosphorylation of endogenous substrates for the two enzyme systems was effectively inhibited by palmitoylcarnitine. When histone was used as exogenous substrate, the carnitine ester inhibited the cardiac phospholipid-sensitive Ca2+-dependent protein kinase but not the cardiac cyclic AMP-dependent and cyclic GMP-dependent protein kinases. It is suggested that inhibition of the Ca2+-dependent phosphorylation of cardiac proteins, regulated by either phospholipid or calmodulin, is probably related in part to the great increase in this fatty acid metabolic intermediate in the ischemic heart.

Animals↗
PubMed1996

Hormone-sensitive lipase is structurally related to acetylcholinesterase, bile salt-stimulated lipase, and several fungal lipases. Building of a three-dimensional model for the catalytic domain of hormone-sensitive lipase.

Hormone-sensitive lipase is the key enzyme in the mobilization of fatty acids from adipose tissue, thereby playing a crucial role in the overall energy homeostasis in mammals. Its activity is stimulated by catecholamines through cAMP-dependent phosphorylation of a single serine, a process that is prevented by insulin. This regulatory property is unique to this enzyme among all known lipases and has been acquired during evolution through insertion of a regulatory module into an ancestral lipase. Sequence alignments have failed to detect significant homology between hormone-sensitive lipase and the rest of the mammalian lipases and esterases, to which this enzyme is only very distantly related. In the present work, we report the finding of a remarkable secondary structure homology between hormone-sensitive lipase and the enzymes from a superfamily of esterases and lipases that includes acetylcholinesterase, bile salt-stimulated lipase, and several fungal lipases. This finding, based on the identification of the secondary structure elements in the hormone-sensitive lipase sequence, has allowed us to construct a three-dimensional model for the catalytic domain of hormone-sensitive lipase. The model reveals the topological organization, predicts the components of the catalytic triad, suggests a three-dimensional localization of the regulatory module, and provides a valuable tool for the future study of structural and functional aspects of this metabolically important enzyme.

Acetylcholinesterase↗
PubMed2000

ATP modulation of ATP-sensitive potassium channel ATP sensitivity varies with the type of SUR subunit.

ATP-sensitive potassium (K(ATP)) channels comprise Kir and SUR subunits. Using recombinant K(ATP) channels expressed in Xenopus oocytes, we observed that MgATP (100 microm) block of Kir6.2/SUR2A currents gradually declined with time, whereas inhibition of Kir6.2/SUR1 or Kir6.2DeltaC36 currents did not change. The decline in Kir6.2/SUR2A ATP sensitivity was not observed in Mg(2+) free solution and was blocked by the phosphatidylinositol (PI) 3-kinase inhibitors LY 294002 (10 microm) and wortmannin (100 microm), and by neomycin (100 microm). These results suggest that a MgATP-dependent synthesis of membrane phospholipids produces a secondary decrease in the ATP sensitivity of Kir6.2/SUR2A. Direct application of the phospholipids PI 4,5-bisphosphate and PI 3,4,5-trisphosphate in the presence of 100 microm MgATP activated all three types of channel, but the response was faster for Kir6.2/SUR2A. Chimeric studies indicate that the different responses of Kir6.2/SUR2A and Kir6.2/SUR1 are mediated by the first six transmembrane domains of SUR. The MgATP-dependent loss of ATP sensitivity of Kir6.2/SUR2A was enhanced by the actin filament disrupter cytochalasin and blocked by phalloidin (which stabilizes the cytoskeleton). Phalloidin did not block the effect of PI 3,4,5-trisphosphate. This suggests that MgATP may cause disruption of the cytoskeleton, leading to enhanced membrane phospholipid levels (or better targeting to the K(ATP) channel) and thus to decreased channel ATP sensitivity.

ATP-Binding Cassette Transporters↗
PubMed2002

Inhibition of deactivation of NO-sensitive guanylyl cyclase accounts for the sensitizing effect of YC-1.

Many of the physiological effects of the signaling molecule nitric oxide are mediated by the stimulation of the NO-sensitive guanylyl cyclase. Activation of the enzyme is achieved by binding of NO to the prosthetic heme group of the enzyme and the initiation of conformational changes. So far, the rate of NO dissociation of the purified enzyme has only been determined spectrophotometrically, whereas the respective deactivation, i.e. the decline in enzymatic activity, has only been determined in cytosolic fractions and intact cells. Here, we report on the deactivation of purified NO-sensitive guanylyl cyclase determined after addition of the NO scavenger oxyhemoglobin or dilution. The deactivation rate corresponded to a half-life of the NO/guanylyl cyclase complex of approximately 4 s, which is in good agreement with the spectrophotometrically measured NO dissociation rate of the enzyme. The deactivation rate of the enzyme determined in platelets yielded a much shorter half-life indicating either partial damage of the enzyme during the purification procedure or the existence of endogenous deactivation accelerating factors. YC-1, a component causing sensitization of guanylyl cyclase toward NO, inhibited deactivation of guanylyl cyclase, resulting in an extremely prolonged half-life of the NO/guanylyl cyclase complex of more than 10 min. The deactivation of an ATP-utilizing guanylyl cyclase mutant was almost unaffected by YC-1, indicating the existence of a special structure within the catalytic domain required for YC-1 binding or for the transduction of the YC-1 effect. In contrast to the wild type enzyme, YC-1 did not increase NO sensitivity of this mutant, clearly establishing inhibition of deactivation as the underlying mechanism of the NO sensitizer YC-1.

Animals↗
PubMedDate not supplied

Pressure pain sensitivity and hardness along human normal and sensitized muscle.

The spatial distribution of pressure sensitivity and muscle hardness was examined on normal muscle tissue and muscle tissue after induction of delayed onset muscle soreness (DOMS). The pressure sensitivity and muscle hardness were assessed at nine sites on the tibialis muscle from the proximal to distal tendon on two separate days. In total 37 healthy volunteers participated in three experiments. In the first experiment pressure pain threshold (PPT) and pressure pain tolerance (PPTO) were assessed. Decreased PPT and PPTO were found on day 2, 7 days after day 1. Proximal and distal stimulation sites were harder compared to muscle belly sites. In a second experiment two different probe sizes were used. Variation in PPT between the nine sites was found for the large probe with muscle belly being less sensitive to pressure stimulation compared to proximal and distal sites. The most proximal stimulation site was harder compared to muscle belly sites. In a third experiment PPT and muscle hardness were assessed before and 48 h after eccentric exercise. PPT at two muscle belly sites was significantly decreased during DOMS. No specific sites were harder during DOMS, the average muscle hardness across sites was however significantly increased. Decreased PPT and increased muscle hardness did not correlate. In conclusion, within subjects the pressure sensitivity varies along the musculoskeletal unit. In DOMS, specific muscle belly sites were more sensitive to pressure stimulation. Muscle-tendon sites were harder compared to muscle belly sites.

Adult↗
PubMed1992

The inherent cellular sensitivity to 62.5 MeV(p----Be+) neutrons of human cells differing in photon sensitivity.

The inherent sensitivity of 20 human cell lines to the 62.5 MeV(p----Be+) clinical neutron beam at Clatterbridge, UK, has been assessed and compared to their sensitivity to 4 MeV photons. The survival curves of the cell lines following neutron irradiation were curvilinear, and the inherent neutron sensitivity varied by 4.5 fold (0.1 survival level) between the extreme values, in the cell lines studied. There was a strong correlation between the sensitivity of these human cells to photon and neutron irradiation. It was concluded that should these in vitro patterns occur in the clinic, the 4-fold variation in RBE and inherent sensitivity to neutrons could result in overall lower local control rates following fast neutron therapy than might be anticipated. It suggests the need for the development of predictive assays as a potential means of selecting tumours most appropriate for neutron therapy.

Cell Line↗
PubMed1953

Studies on the antibodies in rabbit antisera responsible for sensitization of human skin. I. The role of impurities in crystalline egg albumin in stimulating the production of skin-sensitizing antibody.

The capacity of rabbit anti-egg albumin sera to sensitize human skin has been studied. It has been shown that passive transfer by these sera is completely unrelated to the egg albumin-anti-egg albumin system, as demonstrated by a failure of passive transfer by some antisera containing ample anti-egg albumin and persistence of passive transfer in other antisera from which all anti-egg albumin had been removed by precipitation with homologous antigen. Three preparations of non-precipitating anti-egg albumin have been shown to have sensitizing capacities which bear no relation to their non-precipitating anti-egg albumin contents. From a portion of one of these the non-precipitating anti-egg albumin was removed without impairing its sensitizing ability, while in another portion obliteration of the sensitizing capacity was accomplished without reducing the anti-egg albumin. Evidence is presented to show that there are at least two possible antibodies in anti-egg albumin sera which are capable of inducing skin sensitivity and that they are antibodies against egg white impurities in crystalline egg albumin other than anti-conalbumin, anti-ovomucoid, and anti-lysozyme. The usefulness of a suitable quantitative precipitin technic for the analysis for antibodies against antigen impurities and for their selective absorption from sera is illustrated. The principle governing the procedure is described. The technic allows for the determination of a given trace antibody by working with such small concentrations of its purified specific antigen that whatever other antigen-antibody compounds are formed simultaneously with that to be determined will be below their solubility levels and consequently will not contribute appreciably to the precipitate.

Albumins↗
PubMed1990

Radioresistant derivatives of an X-ray-sensitive CHO cell line exhibit distinct patterns of sensitivity to DNA-damaging agents.

X-ray-resistant clones of the xrs-5 radiosensitive derivative of the CHO-K1 cell line were generated by transfecting cosmid library DNAs into the X-ray-sensitive cells. Transfectants were selected for both a dominant drug resistance marker present in the vector sequences and return to wild-type survival. Three cell lines were isolated which show X-ray survival characteristics similar to parental K1 cells. These revertant lines were examined for their cross-sensitivity to cis-diamminedichloroplatinum(II) (cisplatin) and bleomycin. Although these cell lines reverted with regard to X-ray sensitivity, they retained their sensitivity to cisplatin. Furthermore, changes in bleomycin and X-ray sensitivity did not correlate. There was a positive correlation between return to wild-type radiosensitivity and an increase in the rate of DNA double-strand break rejoining.

Animals↗
PubMed1977

Temperature-sensitive mutants of Streptococcus pneumoniae. I. Preparation and characterization in vitro of temperature-sensitive mutants of type I S. pneumoniae.

After exposure of type I Streptococcus pneumoniae to nitrosoguanidine, 13 temperature-sensitive (ts) mutants were selected that were restricted in capacity to form colonies on blood agar at 38 C. Whereas colony formation by the type I parent (ts+) was unaffected by a temperature of as high as 39 C, the ts mutants exhibited a spectrum of temperature sensitivity in which colony formation was inhibited significantly at 36 C, 37 C, 38 C, or 39 C. Growth of ts mutants at 38 C in broth was reduced or delayed relative to that of ts organisms under identical conditions. In general, there was a direct correlation between degree of temperature sensitivity and genetic stability. Mutants grown at a permissive temperature resembled the ts+ type I parent in colonial morphology and properties of alpha-hemolysis, bile solubility, optochin sensitivity, and antibiotic sensitivity. Moreover, in vitro studies indicated that the mutants retained capsules of immunochemically reactive type I capsular polysaccharide.

Bile↗
PubMed1988

Dose-response studies of intracerebroventricular infusion of aldosterone in sensitized and non-sensitized rats.

We have shown previously that the intracerebroventricular (icvt) infusion of 5 ng/h aldosterone (ALD) in the sensitized rat (one kidney removed, 1% NaCl plus 0.15% KCl solution to drink) produced hypertension similar in amplitude and time of onset to a 100-fold dose administered subcutaneously (s.c.), while a 5-ng/h subcutaneous infusion had no effect on blood pressure (BP). Dose-response studies on the icvt infusion of ALD were carried out in sensitized and non-sensitized (intact, with tap water to drink) male Sprague-Dawley rats (SDR). In both studies, a control group received the diluent, artificial cerebrospinal fluid (CSF), icvt. In sensitized rats, the pressures became significantly (P less than 0.05) elevated at day 7 in those receiving 15 ng/h icvt, day 11 in those receiving 5 ng/h icvt and 500 ng/h s.c. and day 18 in those receiving 1.5 ng/h icvt. The indirect systolic BPs at day 20 of infusion were 119 +/- 0.8 (s.e.) mmHg for controls, 182 +/- 5 for 15 ng/h icvt, 140 +/- 2 mmHg for 5 ng/h icvt, 131 +/- 1 mmHg for 1.5 ng/h icvt, 125 +/- 1 mmHg for 0.5 ng/h, and 159 +/- 5 mmHg for 500 ng/h s.c. Recovery (removal of pumps and return to water to drink) for 18 days resulted in the return of normal pressures in all groups except the 15 ng/h, icvt group in which pressures remained slightly, but significantly elevated at 127 +/- 3 mmHg. In non-sensitized rats, the pressures became significantly elevated in animals receiving 45 ng/h icvt and 1 microgram/h s.c. by day 14.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed2000

Context determines the type of sensitized behaviour: a brief review and a hypothesis on the role of environment in behavioural sensitization.

Behavioural sensitization to psychostimulants may develop context-dependency in certain circumstances. Animals given a stimulant repeatedly in a test cage but not in other environments may show enhanced drug-induced behaviour in the test cage. Conditioning mechanisms have been claimed to be responsible for these phenomena. However, several recent findings are not properly accounted for by conditioning. In addition, growing evidence supports the hypothesis that behavioural sensitization reflects neural changes induced by repeated exposure to psychostimulants (the pharmacological hypothesis). However, the pharmacological hypothesis itself fails to account for environmental influences. In this paper, we propose a hypothesis on the role of environment that is complementary to the pharmacological hypothesis. According to our hypothesis, environment does not have a causal role in the development of sensitization, but it modifies the mode of expression of the sensitized behaviour. Sensitization primarily reflects a neuroadaptive change induced by repeated exposure of the neural system to psychostimulants. However, psychostimulants are known to induce different behaviours in different environments. Therefore, repeated administration of a psychostimulant in different environments would result in augmentation of different behaviours. Our hypothesis potentially accommodates various previous observations. We briefly review the literature and present our hypothesis.

Adaptation, Physiological↗
PubMed2004

Allogeneic sensitization is more effective than xenogeneic sensitization in eliciting Gal-mediated skin graft rejection.

The generation of Gal knockout (KO) pigs is likely to be an important advance in xenotransplantation. However, recent reports suggesting that expression of Gal may not be completely eliminated raise the possibility of a continuing anti-Gal immune response. The authors used a Gal-mismatched skin graft model to study cell-mediated anti-Gal rejection. Gal KO mice on a BALB/c or C57BL/6 background were sensitized with allogeneic or xenogeneic (rat) Gal-positive skin grafts and underwent transplantation with a secondary skin graft solely mismatched for Gal 21 days later. Most allograft-sensitized recipients rejected the secondary graft (n=26 [96%]) compared with less than half of xenograft-sensitized recipients (n=25 [44%]). An immunoglobulin (Ig) M response was detected in some xenograft-sensitized but not allograft-sensitized recipients. No recipients developed detectable anti-Gal IgG. The authors' findings contrast with previous reports that xenografts are more potent than allografts in eliciting an anti-Gal response and suggest that a predominantly cell-mediated response can mediate rejection.

Animals↗
PubMed1982

Subpopulation of T cells sensitive to natural thymocytotoxic autoantibody (NTA) of New Zealand mice. I. Distinct cytotoxic sensitivity of functional T cell subsets to NTA and anti-thy-1 antibodies.

NZB mice produce a natural thymocytotoxic autoantibody (NTA) capable of specifically injuring thymocytes and T cells. NTA-reactive antigen (NTA-A) shows a different density distribution among T cells, and partial killing with NTA and complement can eliminate T cells bearing NTA-A in high density. Thy-1 antigen is similar to NTA-A in this respect. To determine the effects of NTA and anti-Thy-1 on distinct functional subsets of T cells, Con A-induced suppressor T cell (Con A-Ts) activity against the allogeneic mixed lymphocyte reaction (MLR), responding T cell (TMLR) activity in the allogeneic MLR, and Con A-induced cytotoxic T cell (Con A-Tc) activity were examined simultaneously in BALB/c spleen cells before and after partial elimination of NTA- and anti-Thy-1-sensitive T cells. Treatment with NTA and complement resulted in a marked reduction in Con A-Ts activity, a significant increase in TMLR-activity and a slight and inconstant decrease in Con A-Tc activity. Since Con A-generated T's were much less sensitive to NTA, the NTA-sensitive T cells involved in Con A-Ts activity appear to be precursors or promoters of the Con A-Ts. In contrast, the precursors of Con A-Tc seem to relatively resistant to NTA. The increase in TMLR activity caused by NTA suggests the possibility that NTA is less cytotoxic for TMLR and cytotoxic for some suppressor T cells in allogeneic MLR. The monoclonal anti-Thy-1 antibody showed no such preferential cytotoxic effects on the three T cell functions. The NTA-sensitive T cells, in contrast to anti-Thy-1-sensitive T cells, were reduced gradually during Con A stimulation. All these findings indicate that NTA-A not only differs from Thy-1 antigen but that it appears to be a unique T cell antigen.

Animals↗
PubMed1993

PUVA erythemal sensitivity depends on plasma psoralen concentration and UVA sensitivity.

The variation in erythemal sensitivity of the skin during PUVA therapy with oral 8-methoxypsoralen (8-MOP) was examined by measuring both UVA and PUVA erythemal responses, together with plasma 8-MOP concentration, in 27 patients about to start PUVA therapy for psoriasis. The erythema responses were judged visually, and also measured using a reflectance instrument in order to construct dose-response curves. No significant association was found between the UVA and PUVA minimal erythema responses. The plasma psoralen concentration showed significant association with the slope of the PUVA erythema dose-response curve. The slopes of the UVA and PUVA erythema dose-response curves were significantly associated, and this association became much stronger when allowance was made for plasma psoralen concentration. These results show that erythemal sensitivity during PUVA therapy is related to both plasma psoralen concentration and inherent UVA sensitivity, but that this relationship is not apparent when sensitivity is judged visually as the minimal erythema response. The association between PUVA and UVA erythemal sensitivity suggests a common pathway in the vascular response induced by UVA radiation, with or without psoralen.

Adult↗
PubMed1998

Prevalence of sensitization to the storage mites Acarus siro, Tyrophagus putrescentiae, and Lepidoglyphus destructor in allergic patients with different degrees of sensitization to the house-dust mite Dermatophagoides pteronyssinus.

The prevalence of sensitization to the storage mites Acarus siro (AS), Tyrophagus putrescentiae (TP), and Lepidoglyphus destructor (LD) was studied in 250 sera of patients with different degrees of sensitization to the house-dust mite Dermatophagoides pteronyssinus (DP) by measuring IgE binding to extracts of the storage mites. Additionally, allergenic cross-reactivity between DP and the storage mite species was studied by RAST inhibition with five individual sera (and a pool of these sera) with moderate IgE levels to all three storage mites and to DP. Increased serum IgE to storage mites was found in 46% of the 200 patients sensitized to DP. Increased prevalence rates of IgE titers to storage mites were associated with higher IgE levels to DP. In 50 sera without sensitization to DP, only five sera showed increased IgE to one of the storage mites. Extracts of TP almost completely inhibited the IgE binding to AS, and vice versa. DP inhibited IgE binding to all storage mites up to 60%, whereas IgE binding to DP was only minimally inhibited by extracts of storage mites. In conclusion, cosensitization to storage mites is a frequent finding in patients sensitized to DP. Although this is largely the result of cross-reactivity between different mite species, it may nevertheless be of clinical significance in patients exposed to storage mites.

Adult↗
PubMed2005

Aspirin-triggered 15-HETE generation in peripheral blood leukocytes is a specific and sensitive Aspirin-Sensitive Patients Identification Test (ASPITest).

BACKGROUND: We have previously demonstrated that aspirin triggers specific generation of 15-hydroxyeicosateraenoic acid (15-HETE) from nasal polyp epithelial cells and peripheral blood leukocytes (PBL) from aspirin-sensitive (AS) but not aspirin-tolerant (AT) patients with asthma/rhinosinusitis. The goal of this study was to assess the diagnostic value of ASA-induced 15-HETE generation measurement to identify AS patients. METHODS: PBL were obtained from 43 AS patients with asthma and rhinosinusitis, 35 AT asthmatics and 17 healthy control (HC) subjects. PBL were incubated with 2-200 muM aspirin (ASA) and 15-HETE release was measured in cell supernatants with competitive ELISA. RESULTS: Unstimulated PBL from all three groups of patients generated similar amount of 15-HETE. Incubation with 200 microM ASA resulted in an increase in an 15-HETE generation (mean increase +421%) in AS-asthmatics but small and nonsignificant response in AT-asthmatics or control subjects. Receiver operating curve (ROC) analysis revealed that the sensitivity of the test for confirmation of ASA-sensitivity was 83% and the specificity 82%. Positive predictive value was 0.79 and negative predictive value was 0.86. Naproxen induced a significant increase in 15-HETE only in some AS-asthmatics, but not in AT-asthmatics. CONCLUSION: Our data demonstrate that ASA-induced 15-HETE generation by PBL is a specific and sensitive aspirin-sensitive patients identification test (ASPITest).

Adult↗