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Symbol:
Aspirin
Alias:
Aspirin; 2-Acetoxybenzenecarboxylic acid; 2-Acetoxybenzoic acid; 2-Carboxyphenyl acetate; 8-hour Bayer; A.S.A.; A.S.A. Empirin; ASA; ASA (VAN); Acenterine; Acesal; Acetal; Acetal (VAN); Aceticyl; Acetilsalicilico; Acetilum acidulatum; Acetisal; Acetol; Acetol (VAN); Acetonyl; Acetophen; Acetosal; Acetosalic acid; Acetosalin; Acetoxybenzoic acid; Acetylin; Acetylsal; Acetylsalicylate; Acetylsalicylic acid; Acetylsalicylsaure; Acetylsalicylsaure (GERMAN); Acetysalicylic acid; Acide acetylsalicylique; Acide acetylsalicylique (FRENCH); Acido O-acetil-benzoico; Acido acetilsalicilico; Acidum acetylsalicylicum; Acimetten; Acisal; Acylpyrin; Adiro; Asagran; Asatard; Ascoden-30; Aspalon; Aspec; Aspergum; Aspirdrops; Aspirin (VAN); Aspirine; Aspro; Asteric; Bayer; Bayer Extra Strength Aspirin For Migraine Pain; Benaspir; Benzoic acid, 2-(acetyloxy)-; Bi-prin; Bialpirina; Bialpirinia; Bufferin; Caprin; Cemirit; Claradin; Clariprin; Colfarit; Contrheuma retard; Coricidin; Crystar; Decaten; Delgesic; Dolean pH 8; Duramax; ECM; Easprin; Ecolen; Ecotrin; Empirin; Endydol; Entericin; Enterophen; Enterosarein; Enterosarine; Entrophen; Extren; Globentyl; Globoid; Helicon; Idragin; Kyselina 2-acetoxybenzoova; Kyselina acetylsalicylova; Levius; Measurin; Micristin; Neuronika; Norgesic; Novid; Nu-seals; Nu-seals aspirin; O-Acetylsalicylic acid; O-accetylsalicylic acid; Persistin; Pharmacin; Pirseal; Polopiryna; Premaspin; Rheumintabletten; Rhodine; Rhonal; Salacetin; Salcetogen; Saletin; Salicylic acid acetate; Salicylic acid, acetate; Salicylic acid, acetyl-; Solfrin; Solprin; Solprin acid; Solpyron; Spira-Dine; St. Joseph; St. Joseph Aspirin for Adults; Supac; Tasprin; Temperal; Triaminicin; Triple-sal; Vanquish; Xaxa; Yasta; o-Acetoxybenzoic acid; o-Carboxyphenyl acetate

Result For Aspirin

Total References : 34797
  • Year: 
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References for year 2010: 341
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Conformationally Gated Fragmentations and Rearrangements Promoted by Interception of the Bergman Cyclization through Intramolecular H-Abstraction: A Possible Mechanism of Auto-Resistance to Natural Enediyne Antibiotics?
PMID:20041688
Author: Baroudi A, Mauldin J, Alabugin IV
Journal: J Am Chem Soc
Affiliation: Department of Chemistry and Biochemistry, Florida State University, Tallahassee, Florida 32306.
  • Abstract
  • Entity
  • Facts
A variety of fragmentations and rearrangements can follow Bergman cyclization in enediynes equipped with acetal rings mimicking the carbohydrate moiety of natural enediyne antibiotics of the esperamicine and calchiamicine families. In the first step of all these processes, intramolecular H-atom abstraction efficiently intercepts the p-benzyne product of the Bergman cyclization through a six-membered TS and transforms the p-benzyne into a new more stable radical. more...
A variety of fragmentations and rearrangements can follow Bergman cyclization in enediynes equipped with acetal rings mimicking the carbohydrate moiety of natural enediyne antibiotics of the esperamicine and calchiamicine families. In the first step of all these processes, intramolecular H-atom abstraction efficiently intercepts the p-benzyne product of the Bergman cyclization through a six-membered TS and transforms the p-benzyne into a new more stable radical. Depending on the substitution pattern and reaction conditions, this radical follows four alternative paths: (a) abstraction of an external hydrogen atom, (b) O-neophyl rearrangement which transposes O- and C-atoms of the substituent, (c) fragmentation of the O-C bond in the acetal ring, or (d) fragmentation with elimination of the appended acetal moiety as a whole. Experiments with varying concentrations of external H-atom donor (1,4-cyclohexadiene) were performed to gain further insight into the competition between intermolecular H-abstraction and the fragmentations. The Thorpe-Ingold effect in gem-dimethyl substituted enediynes enhances the efficiency of fragmentation to the extent where it cannot be prevented even by a large excess of external H-atom donor. These processes provide insight into a possible mechanism of unusual fragmentation of esperamicin A(1) upon its Bergman cycloaromatization and lay foundation for a new approach for the conformational control of reactivity of these natural antitumor antibiotics. Such an approach, in conjunction with supramolecular constraints, may provide a plausible mechanism for resistance to enediyne antibiotics by the enediyne-producing microorganisms. less...
GeneDiseaseDrugProcessesCategories
  • Aspirin
  • Drug based Studies
Depending on the substitution pattern and reaction conditions, this radical follows four alternative paths: (a) abstraction of an external hydrogen atom, (b) O-neophyl rearrangement which transposes O- and C-atoms of the substituent, (c) fragmentation of the O-C bond in the acetal ring, or (d) fragmentation with elimination of the appended acetal moiety as a whole.
GeneDiseaseDrugProcessesCategories
  • Aspirin
  • Drug based Studies
Stereoselective Synthesis of 2-C-Acetonyl-2-Deoxy-d-Galactosides using 1,2-Cyclopropaneacetylated Sugar as Novel Glycosyl Donor.
PMID:20041707
Author: Tian Q, Xu L, Ma X, Zou W, Shao H
Journal: Org Lett
Affiliation: Natural Products Research Center, Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu 610041, China, Institute for Biological Sciences, National Research Council of Canada, 100 Sussex Drive, Ottawa, Ontario K1A 0R6, Canada and Graduate School of Chinese Academy of Sciences, China.
  • Abstract
  • Entity
  • Facts
1,2-Cyclopropaneacetylated sugar is an effective glycosyl donor, which reacted with various glycosyl acceptors including monosaccharides, amino acids and other alcohols in the presence of BF(3)*OEt(2) or TMSOTf. The glycosylation is stereoselective in favor of beta-anomeric products with BF(3)*OEt(2) as catalyst, whereas TMSOTf-catalyzed glycosylation prefers the alpha-anomeric products. more...
1,2-Cyclopropaneacetylated sugar is an effective glycosyl donor, which reacted with various glycosyl acceptors including monosaccharides, amino acids and other alcohols in the presence of BF(3)*OEt(2) or TMSOTf. The glycosylation is stereoselective in favor of beta-anomeric products with BF(3)*OEt(2) as catalyst, whereas TMSOTf-catalyzed glycosylation prefers the alpha-anomeric products. 2-C-Acetonyl-2-deoxy-d-galactosides were obtained in good yields. less...
GeneDiseaseDrugProcessesCategories
  • Aspirin
ACETYLSALICYLIC ACID ENHANCES PURINERGIC RECEPTOR-MEDIATED OUTWARD CURRENTS IN RAT MEGAKARYOCYTES.
PMID:20042731
Author: Young JP, Beckerman J, Vicini S, Myers A
Journal: Am J Physiol Cell Physiol
Affiliation: 1Georgetown University.
  • Abstract
  • Entity
  • Facts
Purinergic receptor activation increases [Ca(++)]i in a fluctuating fashion, triggering oscillatory outward Ca(++) activated K+ currents in rat megakaryocytes (MKs). Whole cell and nystatin perforated patch clamp techniques were used to analyze changes in ionic conductance in MK with acetylsalicylic acid (ASA), a COX-1 inhibitor and antithrombotic agent. more...
Purinergic receptor activation increases [Ca(++)]i in a fluctuating fashion, triggering oscillatory outward Ca(++) activated K+ currents in rat megakaryocytes (MKs). Whole cell and nystatin perforated patch clamp techniques were used to analyze changes in ionic conductance in MK with acetylsalicylic acid (ASA), a COX-1 inhibitor and antithrombotic agent. MKs are a model for platelet reactivity, particularly in ASA treatment failure (ASA resistance). Freshly isolated MKs were incubated 30 min in the absence or presence of 1mM ASA. Using a K(+) rich internal solution, outward currents were recorded in response to 10 muM ATP, 10 muM ADP and 5 muM 2MeSADP in the voltage clamp mode. Agonist-induced currents decreased in amplitude over time, but this decline was attenuated by ASA in both continuous and repeated agonist challenge, indicating increased MK reactivity with ASA treatment. In separate experiments heterologous desensitization was observed when MKs were stimulated with ADP after exposure to a thromboxane receptor agonist (U46619) indicating cross-talk between thromboxane and purinergic pathways. Different cells, treated with ASA or MRS2179 (P2Y1 receptor antagonist), were stimulated with 2MeSADP. The dose response curve was shifted to the left in both cases, suggesting increased MK reactivity. ASA also caused an increased interval between currents (delay). ASA attenuated desensitization of purinergic receptors and increased delay, again suggesting cross-talk between purinergic and thromboxane pathways. These findings may be relevant to ASA resistance, because individual variations in sensitivity to the multiple effects of ASA on signaling pathways could result in insensitivity to its antiplatelet effects in some patients. less...
GeneDiseaseDrugProcessesCategories
  • Aspirin
  • Nystatin
  • Drug based Studies
Whole cell and nystatin perforated patch clamp techniques were used to analyze changes in ionic conductance in MK with acetylsalicylic acid (ASA), a COX-1 inhibitor and antithrombotic agent.
GeneDiseaseDrugProcessesCategories
  • Aspirin
  • Nystatin
  • Drug based Studies
Effect of ampicillin on the bleeding time of neonatal intensive care unit patients.
PMID:20043011
Author: Sheffield MJ, Lambert DK, Henry E, Christensen RD
Journal: J Perinatol
Affiliation: Department of Neonatology, Intermountain Healthcare, McKay-Dee Hospital Center, Ogden, UT, USA.
  • Abstract
  • Entity
  • Facts
Objective:Studies in adults indicate that ampicillin, in a dose-dependent manner, impairs platelet function and moderately prolongs the bleeding time (generally by 60 to 90 s). Unlike aspirin, the inhibition induced by ampicillin involves both reversible and irreversible mechanisms and is not observed immediately after initial dosing (generally requiring approximately 24 h). more...
Objective:Studies in adults indicate that ampicillin, in a dose-dependent manner, impairs platelet function and moderately prolongs the bleeding time (generally by 60 to 90 s). Unlike aspirin, the inhibition induced by ampicillin involves both reversible and irreversible mechanisms and is not observed immediately after initial dosing (generally requiring approximately 24 h). Ampicillin is administered commonly to neonatal intensive care unit (NICU) patients, but its effect on bleeding time in this population has not been reported earlier.Study Design:We performed neonatal template bleeding times and platelet function analyzer (PFA)-100 tests on 15 NICU patients before and at various intervals after intravenous ampicillin dosing.Result:Neonates were only studied if no beta-lactam antibiotics were administered to their mother during labor, and if they had ampicillin ordered by the clinician at a dose of 50 to 100 mg kg(-1) every 12 h. Subjects ranged from 33 to 41 weeks gestation and weighed 1760 to 3835 g. Bleeding times before the first ampicillin dose (n=15) averaged 134 s (95% confidence interval (CI), 120 to 148 s) and PFA-100 times averaged 123 s (95% CI, 96 to 149 s). After the first dose of ampicillin (n=5), bleeding times and PFA-100 times did not increase, but after the third (n=5) and fourth doses (n=4) bleeding times lengthened by an average of 60 s (95% CI, 37 to 83 s, P<0.001) and PFA-100 times lengthened by an average of 20 s (95% CI, -20 to 60 s, P=0.15).Conclusion:Ampicillin administered intravenously to NICU patients prolongs the bleeding time, with a magnitude-of-effect and time-to-effect similar to that shown earlier in adults.Journal of Perinatology advance online publication, 31 December 2009; doi:10.1038/jp.2009.192. less...
GeneDiseaseDrugProcessesCategories
  • Hemorrhage
  • Ampicillin
  • Aspirin
  • Drug based Studies
Effect of ampicillin on the bleeding time of neonatal intensive care unit patients.
GeneDiseaseDrugProcessesCategories
  • Hemorrhage
  • Ampicillin
  • Drug based Studies
Objective:Studies in adults indicate that ampicillin, in a dose-dependent manner, impairs platelet function and moderately prolongs the bleeding time (generally by 60 to 90 s).
GeneDiseaseDrugProcessesCategories
  • Hemorrhage
  • Ampicillin
  • Drug based Studies
Unlike aspirin, the inhibition induced by ampicillin involves both reversible and irreversible mechanisms and is not observed immediately after initial dosing (generally requiring approximately 24 h).
GeneDiseaseDrugProcessesCategories
  • Ampicillin
  • Aspirin
  • Drug based Studies
Ampicillin is administered commonly to neonatal intensive care unit (NICU) patients, but its effect on bleeding time in this population has not been reported earlier.Study Design:We performed neonatal template bleeding times and platelet function analyzer (PFA)-100 tests on 15 NICU patients before and at various intervals after intravenous ampicillin dosing.Result:Neonates were only studied if no beta-lactam antibiotics were administered to their mother during labor, and if they had ampicillin ordered by the clinician at a dose of 50 to 100 mg kg(-1) every 12 h.
GeneDiseaseDrugProcessesCategories
  • Hemorrhage
  • Ampicillin
  • Drug based Studies
Bleeding times before the first ampicillin dose (n=15) averaged 134 s (95% confidence interval (CI), 120 to 148 s) and PFA-100 times averaged 123 s (95% CI, 96 to 149 s).
GeneDiseaseDrugProcessesCategories
  • Hemorrhage
  • Ampicillin
  • Drug based Studies
After the first dose of ampicillin (n=5), bleeding times and PFA-100 times did not increase, but after the third (n=5) and fourth doses (n=4) bleeding times lengthened by an average of 60 s (95% CI, 37 to 83 s, P<0.001) and PFA-100 times lengthened by an average of 20 s (95% CI, -20 to 60 s, P=0.15).Conclusion:Ampicillin administered intravenously to NICU patients prolongs the bleeding time, with a magnitude-of-effect and time-to-effect similar to that shown earlier in adults.Journal of Perinatology advance online publication, 31 December 2009; doi:10.1038/jp.2009.192.
GeneDiseaseDrugProcessesCategories
  • Hemorrhage
  • Ampicillin
  • Drug based Studies
Long-term administration of aspirin inhibits tumour formation and triggers anti-neoplastic molecular changes in a pre-clinical model of colon carcinogenesis.
PMID:20043115
Author: Bousserouel S, Gosse F, Bouhadjar M, Soler L, Marescaux J, Raul F
Journal: Oncol Rep
Affiliation: University of Strasbourg Unit EA 4438, Faculty of Medicine, Laboratory of Nutritional Cancer Prevention, Strasbourg, France.
  • Abstract
  • Entity
  • Facts
Despite numerous studies aimed at verifying the anti-tumour activity of aspirin on colon carcinogenesis little is known on the molecular targets involved in the anti-carcinogenic properties of this drug. We investigated the long-term administration of low dose of aspirin in a model of experimental colon carcinogenesis in rats. more...
Despite numerous studies aimed at verifying the anti-tumour activity of aspirin on colon carcinogenesis little is known on the molecular targets involved in the anti-carcinogenic properties of this drug. We investigated the long-term administration of low dose of aspirin in a model of experimental colon carcinogenesis in rats. Adult Wistar rats received an intraperitoneal injection of azoxymethane (AOM) once a week for two weeks in order to initiate colon carcinogenesis. One week after AOM injection, rats received daily 0.01% aspirin (6 mg/kg body weight) in drinking water for 10 months. Compared to AOM control rats, aspirin treatment for 10 months caused a 50% reduction of the number of aberrant crypt foci associated with a 50% reduction of prostaglandin E2 (PGE2) concentration and suppressed by 80% tumour formation in the colon. RT-PCR quantitative analysis showed that aspirin treatment reduced significantly (P<0.01) the AOM-triggered increase in mRNA levels of soluble inflammatory mediators (TNFalpha and IL-1beta) and metalloproteinases (MMP3 and MMP7). Conversely, we detected an increased expression level of alpha-defensin-5 (Rd-5, 2 fold) and lipocalin-2 (LCN2, 4 fold), two markers of the innate immunity system. The expression of apoptosis-related genes such as death receptors and their ligands were reduced by aspirin and the Bcl-2/Bax transcript ratio droped, Bcl-2 expression being reduced to the level found in saline control rats. The present study identifies new molecular targets triggered by aspirin in the colonic mucosa and may support the use of non-toxic low dose of aspirin in long-term treatments as a prophylactic approach against colon carcinogenesis. less...
GeneDiseaseDrugProcessesCategories
  • BAX_HUMAN
  • DEF5_HUMAN
  • IL1B_HUMAN
  • NGAL_HUMAN
  • MMP3_HUMAN
  • MMP7_HUMAN
  • BCL2_HUMAN
  • TNFA_HUMAN
  • TUB_HUMAN
  • Aspirin
  • apoptosis
  • Drug based Studies
  • Protein/Gene relationships
We investigated the long-term administration of low dose of aspirin in a model of experimental colon carcinogenesis in rats.
GeneDiseaseDrugProcessesCategories
  • Aspirin
  • Drug based Studies
RT-PCR quantitative analysis showed that aspirin treatment reduced significantly (P<0.01) the AOM-triggered increase in mRNA levels of soluble inflammatory mediators (TNFalpha and IL-1beta) and metalloproteinases (MMP3 and MMP7).
GeneDiseaseDrugProcessesCategories
  • IL1B_HUMAN
  • MMP3_HUMAN
  • MMP7_HUMAN
  • TNFA_HUMAN
  • Aspirin
  • Protein/Gene relationships
Conversely, we detected an increased expression level of alpha-defensin-5 (Rd-5, 2 fold) and lipocalin-2 (LCN2, 4 fold), two markers of the innate immunity system.
GeneDiseaseDrugProcessesCategories
  • DEF5_HUMAN
  • NGAL_HUMAN
  • TUB_HUMAN
  • Protein/Gene relationships
The expression of apoptosis-related genes such as death receptors and their ligands were reduced by aspirin and the Bcl-2/Bax transcript ratio droped, Bcl-2 expression being reduced to the level found in saline control rats.
GeneDiseaseDrugProcessesCategories
  • BAX_HUMAN
  • BCL2_HUMAN
  • Aspirin
  • apoptosis
  • Drug based Studies
  • Protein/Gene relationships
The present study identifies new molecular targets triggered by aspirin in the colonic mucosa and may support the use of non-toxic low dose of aspirin in long-term treatments as a prophylactic approach against colon carcinogenesis.
GeneDiseaseDrugProcessesCategories
  • Aspirin
  • Drug based Studies
Influence of anticoagulants on the appearance of chronic subdural hematoma.
PMID:20043584
Author: Krupa M, Moskała M, Składzień T, Grzywna E
Journal: Przegl Lek
Affiliation: Z Kliniki Neurotraumatologii CM UJ w Krakowie. krupa@cm-uj.krakow.pl
  • Abstract
  • Entity
  • Facts
In recent years in the Department of Neurotraumatology in Cracow it has been noticed the frequent connection between appearance of chronic subdural hematoma (CSDH) and treatment by anticoagulant medications. The aim of this study is to draw attention to the problem of insufficient control of anticoagulants consumption, especially by patients treated for cardiovascular system diseases that increases the risk of bleeding and CSDH development. more...
In recent years in the Department of Neurotraumatology in Cracow it has been noticed the frequent connection between appearance of chronic subdural hematoma (CSDH) and treatment by anticoagulant medications. The aim of this study is to draw attention to the problem of insufficient control of anticoagulants consumption, especially by patients treated for cardiovascular system diseases that increases the risk of bleeding and CSDH development. The paper is based on data from questionnaires that was sent to patients with CSDH, cured in the Department of Neurotraumatology form 2004 to 2005. Analyzed was the group of 51 patients with chronic subdural hematoma; 37 individuals (72.5%) confirmed taking acetylsalicylic acid in the period of 3 months before admission to the Department, 9 (17.6%) patients answered that they were taking low-molecular weight heparin. One patient (1.9%) was taking chronically derivative of cumarin. The authors would inform that anticoagulant treatment might favour increase of chronic subdural hematoma incidence. It's especially important, because the average life expectancy has been prolonged in Poland and there are more people taking acetylsalicylic acid. This can be an epidemiological problem in future. less...
GeneDiseaseDrugProcessesCategories
  • Hematoma, Subdural
  • Hemorrhage
  • Hematoma, Subdural, Chronic
  • Heparin
  • Aspirin
  • Drug based Studies
Analyzed was the group of 51 patients with chronic subdural hematoma; 37 individuals (72.5%) confirmed taking acetylsalicylic acid in the period of 3 months before admission to the Department, 9 (17.6%) patients answered that they were taking low-molecular weight heparin.
GeneDiseaseDrugProcessesCategories
  • Hematoma, Subdural
  • Heparin
  • Aspirin
  • Drug based Studies
Toosendanin: Synthesis of the AB-ring and investigations of its anti-botulinum properties (Part II).
PMID:20044261
Author: Nakai Y, Pellett S, Tepp WH, Johnson EA, Janda KD
Journal: Bioorg Med Chem
Affiliation: Departments of Chemistry and Immunology and The Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
  • Abstract
  • Entity
  • Facts
Botulinum neurotoxins (BoNTs) are the etiological agents responsible for botulism, a disease characterized by peripheral neuromuscular blockade and a characteristic flaccid paralysis of humans. The natural product toosendanin, a limonoid, is a traditional Chinese medicine that has reported anti-botulinum properties in animal models. more...
Botulinum neurotoxins (BoNTs) are the etiological agents responsible for botulism, a disease characterized by peripheral neuromuscular blockade and a characteristic flaccid paralysis of humans. The natural product toosendanin, a limonoid, is a traditional Chinese medicine that has reported anti-botulinum properties in animal models. Toosendanin effectively inhibits the biological activity of BoNT/A in neuronal cells at concentrations of 200nM, and partial inhibition can be observed with concentrations as low as 8nM. Mechanistically, toosendanin's inhibition is due to prevention of transduction of the BoNT LC through the HC channel. Intriguing questions as to the molecular architecture of toosendanin as related to its anti-botulinum properties have focused our attention on a synthesis of toosendanin's unusual AB-ring, containing a unique bridged hemi-acetal. Within the current work, a synthetic strategy allowing access to the AB-fragment of toosendanin was achieved from a trans-decalin system. In addition, this fragment was examined for its modulation of BoNT/A intoxication in a rat spinal cord cellular assay. less...
GeneDiseaseDrugProcessesCategories
  • Botulism
  • Paralysis
  • Botulinum Toxin
  • Aspirin
  • transduction
  • Disease Mechanisms
Botulinum neurotoxins (BoNTs) are the etiological agents responsible for botulism, a disease characterized by peripheral neuromuscular blockade and a characteristic flaccid paralysis of humans.
GeneDiseaseDrugProcessesCategories
  • Botulism
  • Paralysis
  • Disease Mechanisms
Prevalence of Embolic Signals in Acute Coronary Syndromes.
PMID:20044527
Author: Meseguer E, Labreuche J, Durdilly C, Echeverría A, Lavallee PC, Ducrocq G, Touboul PJ, Steg PG, Amarenco P
Journal: Stroke
Affiliation: INSERM U-698 and Paris-Diderot University, Bichat Hospital, Assistance Publique-Hopitaux de Paris, Paris, France.
  • Abstract
  • Entity
  • Facts
BACKGROUND AND PURPOSE: The purpose of this study was to assess the prevalence of embolic signals (ES) in acute coronary syndromes (ACS) and their association with stroke. METHODS: From December 2004 to October 2006, 209 consecutive patients with ACS (without prosthetic heart valves or previous stroke) were studied within 72 hours of symptom onset. more...
BACKGROUND AND PURPOSE: The purpose of this study was to assess the prevalence of embolic signals (ES) in acute coronary syndromes (ACS) and their association with stroke. METHODS: From December 2004 to October 2006, 209 consecutive patients with ACS (without prosthetic heart valves or previous stroke) were studied within 72 hours of symptom onset. Patients underwent ES monitoring in both middle cerebral arteries by transcranial Doppler for 30 minutes. Median follow-up was 14 months after discharge. RESULTS: Patients were treated according to current European Society Cardiology guidelines. Specifically, 92% of patients received heparin(s), 100% aspirin, 92% clopidogrel, 67% intravenous glycoprotein IIb/IIIa inhibitors, 9% fibrinolysis, and 67% underwent angioplasty. ES were detected in 7 patients (prevalence 3.4%; 95% CI, 1.4 to 6.8). Except for a higher prevalence of ES in patients with unstable angina versus other ACS categories (8.5% versus 1.9%, P=0.047), none of the factors among baseline characteristics, clinical features, ACS treatment, and cardiac findings were associated with the presence of ES. During hospitalization, 3 patients without ES had cerebrovascular events (one stroke and 2 transient ischemic attacks), whereas no cerebrovascular events occurred in patients with ES. CONCLUSIONS: The prevalence of ES among hospitalized patients with ACS is currently low, possibly because of improvement in ACS treatment. In this ACS sample, ES did not appear associated with short-term risk of cerebrovascular events. less...
GeneDiseaseDrugProcessesCategories
  • Angina, Unstable
  • Ischemic Attack, Transient
  • Stroke
  • Acute Coronary Syndrome
  • Clopidogrel
  • Aspirin
  • Heparin
  • fibrinolysis
  • Disease Mechanisms
  • Drug based Studies
BACKGROUND AND PURPOSE: The purpose of this study was to assess the prevalence of embolic signals (ES) in acute coronary syndromes (ACS) and their association with stroke.
GeneDiseaseDrugProcessesCategories
  • Stroke
  • Acute Coronary Syndrome
  • Disease Mechanisms
Specifically, 92% of patients received heparin(s), 100% aspirin, 92% clopidogrel, 67% intravenous glycoprotein IIb/IIIa inhibitors, 9% fibrinolysis, and 67% underwent angioplasty.
GeneDiseaseDrugProcessesCategories
  • Clopidogrel
  • Aspirin
  • Heparin
  • fibrinolysis
  • Drug based Studies
During hospitalization, 3 patients without ES had cerebrovascular events (one stroke and 2 transient ischemic attacks), whereas no cerebrovascular events occurred in patients with ES.
GeneDiseaseDrugProcessesCategories
  • Ischemic Attack, Transient
  • Stroke
  • Disease Mechanisms
Comparison between single antiplatelet therapy and combination of antiplatelet and anticoagulation therapy for secondary prevention in ischemic stroke patients with antiphospholipid syndrome.
PMID:20046230
Author: Okuma H, Kitagawa Y, Yasuda T, Tokuoka K, Takagi S
Journal: Int J Med Sci
Affiliation: Department of Neurology, Tokai University Tokyo Hospital, Tokyo, Japan. ookuma@tok.u-tokai.ac.jp
  • Abstract
  • Entity
  • Facts
Satisfactory results have not yet been obtained in therapy for secondary prevention in ischemic stroke patients with antiphospholipid syndrome (APS). We therefore compared single antiplatelet therapy and a combination of antiplatelet and anticoagulation therapy for secondary prevention in ischemic stroke patients with APS.The subjects were 20 ischemic stroke patients with antiphospholipid antibody, 13 with primary antiphospholipid syndrome and 7 with SLE-related antiphospholipid syndrome. more...
Satisfactory results have not yet been obtained in therapy for secondary prevention in ischemic stroke patients with antiphospholipid syndrome (APS). We therefore compared single antiplatelet therapy and a combination of antiplatelet and anticoagulation therapy for secondary prevention in ischemic stroke patients with APS.The subjects were 20 ischemic stroke patients with antiphospholipid antibody, 13 with primary antiphospholipid syndrome and 7 with SLE-related antiphospholipid syndrome. Diagnosis of APS was based on the 2006 Sydney criteria. Eligible patients were randomly assigned to either single antiplatelet therapy (aspirin 100 mg) or a combination of antiplatelet and anticoagulation therapy (target INR: 2.0-3.0; mean 2.4+/-0.3) for the secondary prevention of stroke according to a double-blind protocol. There was no significant difference between the two groups in age, gender, NIH Stroke Scale on admission, mRS at discharge, or rate of hypertension, diabetes mellitus, hyperlipidemia, or cardiac disease. We obtained Kaplan-Meier survival curves for each treatment. The primary outcome was the occurrence of stroke. The mean follow-up time was 3.9+/-2.0 years. The cumulative incidence of stroke in patients with single antiplatelet treatment was statistically significantly higher than that in patients receiving the combination of antiplatelet and anticoagulation therapy (log-rank test, p-value=0.026). The incidence of hemorrhagic complications was similar in the two groups. The recent APASS study did not show any difference in effectiveness for secondary prevention between single antiplatelet (aspirin) and single anticoagulant (warfarin) therapy. Our results indicate that combination therapy may be more effective in APS-related ischemic stroke. less...
GeneDiseaseDrugProcessesCategories
  • Diabetes Mellitus
  • Heart Diseases
  • Hyperlipidemias
  • Hypertension
  • Antiphospholipid Syndrome
  • Stroke
  • Aspirin
  • Warfarin
  • Disease Mechanisms
  • Drug based Studies
Comparison between single antiplatelet therapy and combination of antiplatelet and anticoagulation therapy for secondary prevention in ischemic stroke patients with antiphospholipid syndrome.
GeneDiseaseDrugProcessesCategories
  • Antiphospholipid Syndrome
  • Stroke
  • Disease Mechanisms
Satisfactory results have not yet been obtained in therapy for secondary prevention in ischemic stroke patients with antiphospholipid syndrome (APS).
GeneDiseaseDrugProcessesCategories
  • Antiphospholipid Syndrome
  • Stroke
  • Disease Mechanisms
We therefore compared single antiplatelet therapy and a combination of antiplatelet and anticoagulation therapy for secondary prevention in ischemic stroke patients with APS.The subjects were 20 ischemic stroke patients with antiphospholipid antibody, 13 with primary antiphospholipid syndrome and 7 with SLE-related antiphospholipid syndrome.
GeneDiseaseDrugProcessesCategories
  • Antiphospholipid Syndrome
  • Stroke
  • Disease Mechanisms
Eligible patients were randomly assigned to either single antiplatelet therapy (aspirin 100 mg) or a combination of antiplatelet and anticoagulation therapy (target INR: 2.0-3.0; mean 2.4+/-0.3) for the secondary prevention of stroke according to a double-blind protocol.
GeneDiseaseDrugProcessesCategories
  • Stroke
  • Aspirin
  • Disease Mechanisms
  • Drug based Studies
There was no significant difference between the two groups in age, gender, NIH Stroke Scale on admission, mRS at discharge, or rate of hypertension, diabetes mellitus, hyperlipidemia, or cardiac disease.
GeneDiseaseDrugProcessesCategories
  • Diabetes Mellitus
  • Heart Diseases
  • Hyperlipidemias
  • Hypertension
  • Stroke
  • Disease Mechanisms
The cumulative incidence of stroke in patients with single antiplatelet treatment was statistically significantly higher than that in patients receiving the combination of antiplatelet and anticoagulation therapy (log-rank test, p-value=0.026).
GeneDiseaseDrugProcessesCategories
  • Stroke
  • Disease Mechanisms
The recent APASS study did not show any difference in effectiveness for secondary prevention between single antiplatelet (aspirin) and single anticoagulant (warfarin) therapy.
GeneDiseaseDrugProcessesCategories
  • Aspirin
  • Warfarin
  • Disease Mechanisms
  • Drug based Studies
Our results indicate that combination therapy may be more effective in APS-related ischemic stroke.
GeneDiseaseDrugProcessesCategories
  • Stroke
  • Disease Mechanisms
Update on recent advances in the management of aspirin exacerbated respiratory disease.
PMID:20046412
Author: Palikhe NS, Kim JH, Park HS
Journal: Yonsei Med J
Affiliation: Department of Allergy and Rheumatology, Ajou University School of Medicine, Yeongtong-gu, Suwon, Korea.
  • Abstract
  • Entity
  • Facts
Aspirin intolerant asthma (AIA) is frequently characterized as an aspirin (ASA)-exacerbated respiratory disease (AERD). It is a clinical syndrome associated with chronic severe inflammation in the upper and lower airways resulting in chronic rhinitis, sinusitis, recurrent polyposis, and asthma. more...
Aspirin intolerant asthma (AIA) is frequently characterized as an aspirin (ASA)-exacerbated respiratory disease (AERD). It is a clinical syndrome associated with chronic severe inflammation in the upper and lower airways resulting in chronic rhinitis, sinusitis, recurrent polyposis, and asthma. AERD generally develops secondary to abnormalities in inflammatory mediators and arachidonic acid biosynthesis expression. Upper and lower airway eosinophil infiltration is a key feature of AERD; however, the exact mechanisms of such chronic eosinophilic inflammation are not fully understood. Cysteinyl leukotriene over-production may be a key factor in the induction of eosinophilic activation. Genetic studies have suggested a role for variability of genes in disease susceptibility and response to medication. Potential genetic biomarkers contributing to the AERD phenotype include HLA-DPB1*301, LTC4S, ALOX5, CYSLT, PGE2, TBXA2R, TBX21, MS4A2, IL10 -1082A > G, ACE -262A > T, and CRTH2 -466T > C; the four-locus SNP set was composed of B2ADR 46A > G, CCR3 -520T > G, CysLTR1 -634C > T, and FCER1B -109T > C. Management of AERD is an important issue. Aspirin ingestion may result in significant morbidity and mortality, and patients must be advised regarding aspirin risk. Leukotriene receptor antagonists (LTRA) that inhibit leukotriene pathways have an established role in long-term AERD management and rhinosinusitis. Aspirin desensitization may be required for the relief of upper and lower airway symptoms in AERD patients. Future research should focus on identification of biomarkers for a comprehensive diagnostic approach. less...
GeneDiseaseDrugProcessesCategories
  • HB2P_HUMAN
  • LTC4S_HUMAN
  • FCERB_HUMAN
  • LOX5_HUMAN
  • TBX21_HUMAN
  • TA2R_HUMAN
  • Asthma
  • Inflammation
  • Rhinitis
  • Sinusitis
  • Aspirin
  • Arachidonic Acid
  • Drug based Studies
  • Disease Mechanisms
  • Protein/Gene relationships
Aspirin intolerant asthma (AIA) is frequently characterized as an aspirin (ASA)-exacerbated respiratory disease (AERD).
GeneDiseaseDrugProcessesCategories
  • Asthma
  • Aspirin
  • Drug based Studies
It is a clinical syndrome associated with chronic severe inflammation in the upper and lower airways resulting in chronic rhinitis, sinusitis, recurrent polyposis, and asthma.
GeneDiseaseDrugProcessesCategories
  • Asthma
  • Inflammation
  • Rhinitis
  • Sinusitis
  • Disease Mechanisms
Potential genetic biomarkers contributing to the AERD phenotype include HLA-DPB1*301, LTC4S, ALOX5, CYSLT, PGE2, TBXA2R, TBX21, MS4A2, IL10 -1082A > G, ACE -262A > T, and CRTH2 -466T > C; the four-locus SNP set was composed of B2ADR 46A > G, CCR3 -520T > G, CysLTR1 -634C > T, and FCER1B -109T > C.
GeneDiseaseDrugProcessesCategories
  • HB2P_HUMAN
  • LTC4S_HUMAN
  • FCERB_HUMAN
  • LOX5_HUMAN
  • TBX21_HUMAN
  • TA2R_HUMAN
  • Protein/Gene relationships


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