Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.1 (ACS)
 78,556 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to determine the safety and efficacy of the second-generation ACS Multi-Link Duet coronary stent system for the treatment of single, symptomatic, de novo, native coronary artery lesions. Between February and June 1998, 427 patients (69.3% male, 51.5% class 3 or 4 angina, 20.1% diabetic, 43.6% hyperlipidemia) were included at 38 centers in this prospective observational study. All patients received ticlopidine 500 mg/day for 1 month and aspirin > or =100 mg/day. The Duet stent was available in 8, 18, and 28 mm length and 3.0, 3.5, and 4.0 mm diameter. After adequate predilatation, stents were successfully implanted, at up to 16 atm, in 99.3% of patients. Mean vessel diameter by core laboratory quantitative coronary angiography was 3.0 +/- 0.53 mm and postprocedural minimum luminal diameter was 2.79 +/- 0.43 mm (12% +/- 9.3% diameter stenosis). At 30 days, 96.7% of patients were event-free and at 6 months 88.1% remained free of major adverse cardiac events. The restenosis rate was 18.1%. The ACS Duet stent was safely implanted in >99% of target lesions by a diverse group of international investigators. With late outcomes at least comparable to the best published results, this stent platform provides safe and effective percutaneous treatment of obstructive coronary artery disease. Cathet Cardiovasc Intervent 2001;54:25-33.
Catheter Cardiovasc Interv 2001 Sep
PMID:Acute and 6-month clinical and angiographic outcome after implantation of the ACS Duet stent for single-vessel coronary artery disease: final results of the European and US ACS Multi-link Duet Registry. 1155 44

We compared troponin I (TnI) assays (AxSYM [Abbott]; ACS:180 [Bayer]) in blood samples with concentrations less than 10 ng/mL (< 10 micrograms/L). Discordant results were evaluated by linearity studies and by testing for rheumatoid factor. Patients with discordant TnI results were compared with patients with concordant results and patients with negative TnI who had a new myocardial infarction or died within 2 months of initial testing. Positive TnI cutoffs by AxSYM and ACS:180 were 0.7 ng/mL (0.7 microgram/L) and 0.13 ng/mL (0.13 microgram/L), respectively. We identified 173 specimens that were repeatedly positive by at least 1 assay; 143 specimens were positive by both assays. Twenty samples positive for TnI by AxSYM were negative by ACS:180, while 10 samples positive by ACS:180 were negative by AxSYM. The discordant samples showed no evidence of interfering substances, including rheumatoid factor. Clinical follow-up showed that 26% of patients with elevated TnI by both assays, 33% with TnI positive only by AxSYM, 22% with TnI positive only by ACS:180, and 8% with negative TnI by AxSYM encountered at least 1 clinical end point. Variable detection rates by these assays for low-positive TnI represent a clinically significant problem.
Am J Clin Pathol 2001 Sep
PMID:Clinical significance of low-positive troponin I by AxSYM and ACS:180. 1155 68

Fibroblast growth factors are structurally related proteins associated with cell growth, differentiation, migration, wound healing, angiogenesis, and oncogenesis. At the cellular level, their function is mediated by transmembrane tyrosinekinase receptors, fibroblast growth factor receptors. Four genes encoding fibroblast growth factor receptors have been identified, and mutations in three of these, FGFR1, FGFR2, and FGFR3, can cause different congenital, autosomal dominant disorders affecting the craniofacial and skeletal development: craniosynostosis and chondrodysplasias. The craniosynostosis syndromes: Apert syndrome, Beare-Stevenson syndrome, Crouzon syndrome, Jackson-Weiss syndrome, Muenke syndrome, Pfeiffer syndrome and Saethre-Chotzen syndrome can be caused by mutation in either FGFR1, FGFR2, or FGFR3. Saethre-Chotzen syndrome can also be caused by mutation in a functionally related gene, ACS. The same mutation can cause different syndromes, and the same syndrome can be caused by mutations in different genes. The chondrodysplasias: achondroplasia, hypochondroplasia, and thanatophoric dysplasia are all caused by mutations in FGFR3.
Ugeskr Laeger 2001 Sep 03
PMID:[The molecular genetic background of hereditary craniosynostoses and chondrodysplasias]. 1157 61

Despite sonographic detection of foetal goitre, uncertainty persists in the initial diagnosis of thyrotoxicosis and hypothyroidism. The aim of this study was to establish foetal and neonatal iodothyronine and thyrotrophin reference values for the ACS-180SE analyser. From 22 to 36 weeks of gestation, median foetal serum free thyroxine (FT4) levels increased from 6.0 pmol/L to 143 pmol/L, while free tri-iodothyronine (FT3) levels increased from 0.7 pmol/L to 1.9 pmol/L and mean thyrotrophin (TSH) levels remained stable (10.2 +/- 3.8mU/L; n = 33). At birth, concentrations were independent of gender and gestational age. Among the 10 cases of sonographically detected foetal goitre, serum TSH and FT4 were measured in five, showing hypothyroidism (3/5) or hyperthyroidism (2/5). Cord blood TSH levels reflected the efficacy of prenatal therapy. Measurement of foetal FT4 and TSH can be used to confirm foetal thyroid dysfunction, whereas treatment efficacy can be assessed sonographically and confirmed by measurement of TSH assay at birth.
Ann Clin Biochem 2001 Sep
PMID:Biochemical investigation of foetal and neonatal thyroid function using the ACS-180SE analyser: clinical application. 1158 30

The treatment of ACS without persistent ST-segment elevation is evolving. Antiplatelet and antithrombin therapy forms the mainstay of medical management. The antiplatelet agents studied can be pharmacologically classified as GP lIb/IIIa receptor antagonists, ADP receptor antagonists, thromboxane inhibitors, and cyclo-oxygenase inhibitors. While aspirin, a cyclo-oxygenase inhibitor, is well entrenched in the treatment (and thus will not be reviewed here), other drugs have been subjects of intense study and large-scale clinical trials in the last decade. In this article we will explore the rationale of using antiplatelet agents, describe the platelet biology and mechanism of action of these drugs, narrate the major phase III trials, and attempt to draw conclusions from the clinical experience. Important trials which have been presented at principal international scientific meetings and which have not yet been published are also cited.
Cardiovasc Drugs Ther 2001 Sep
PMID:Antiplatelet therapy in acute coronary syndromes without persistent ST-segment elevation. 1185 61

The purpose of this study was to characterize the retention kinetics of recombinant human bone morphogenetic protein-2 (rhBMP-2) applied to two calcium-based delivery matrices. Biphasic calcium phosphate (BCP) and a composite containing BCP in an absorbable collagen sponge (BCP/ACS) were evaluated using a spinal fusion model in rabbits. rhBMP-2 labeled with radioactive iodine (125I) was used as a tracer to assess in vivo retention of rhBMP-2 in the presence of these materials (nine animals per material studied). Over a 36 day study period, animals were assessed for the following: percent administered dose retained at the implant site as measured by scintigraphic imaging (counting) with a gamma camera (all animals), radiography of the implant site (all animals), radioactivity in blood and plasma (all animals), and radioactivity in the urine and feces (three animals for each material). Radioactivity data were corrected for the decay of 125I and the attenuation between the implant in vivo and the gamma camera. Differences observed between the two materials for the area under the retention vs. time profile (AUC; 988%*day for BCP vs. 1070%*day for BCP/ACS, p = 0.57) and the mean residence time (MRT; 10.2 days for BCP vs. 7.6 days for BCP/ACS, p = 0.06) were not statistically significant. Initial retention/incorporation of rhBMP-2 was slightly higher for rhBMP-2/BCP/ACS than for rhBMP-2/BCP (96.8% vs. 86.0%, p < 0.05). Animals receiving rhBMP-2/BCP showed a longer terminal retention half-life (t1/2) than did those receiving rhBMP-2/BCP/ACS (7.5 vs. 4.5 days, p < 0.05). The urinary radioactivity recovery data supported the data obtained by scintigraphy. Over the 36 day collection period, essentially complete recovery of radioactivity (dose) in urine was observed for rhBMP-2/BCP and rhBMP-2/BCP/ACS and the majority of the radioactivity (approximately 95%) was soluble in trichloroacetic acid, suggesting extensive catabolism of rhBMP-2 before renal excretion. Fecal recovery of radioactivity was low, approximately 2-3%. In conclusion, rhBMP-2 was retained at the implant site when delivered with either BCP or BCP/ACS based on mean residence time and area under the retention curve vs. time profile. Use of these matrices resulted in detectable rhBMP-2 levels at the surgical site for over a week in contrast to data reported with several other matrices that lasted less time. Systemic catabolism and elimination of the rhBMP-2 was extensive and systemic presence of the protein was negligible.
J Orthop Res 2002 Sep
PMID:Retention of 125I-labeled recombinant human bone morphogenetic protein-2 by biphasic calcium phosphate or a composite sponge in a rabbit posterolateral spine arthrodesis model. 1238 73

CheY, a response regulator of the chemotaxis system in Escherichia coli, can be activated by either phosphorylation or acetylation to generate clockwise rotation of the flagellar motor. Both covalent modifications are involved in chemotaxis, but the function of the latter remains obscure. To understand why two different modifications apparently activate the same function of CheY, we studied the effect that each modification exerts on the other. The phosphodonors of CheY, the histidine kinase CheA and acetyl phosphate, each strongly inhibited both the autoacetylation of the acetylating enzyme, acetyl-CoA synthetase (Acs), and the acetylation of CheY. CheZ, the enzyme that enhances CheY dephosphorylation, had the opposite effect and enhanced Acs autoacetylation and CheY acetylation. These effects of the phosphodonors and CheZ were not caused by their respective activities. Rather, they were caused by their interactions with Acs and, possibly, with CheY. In addition, the presence of Acs elevated the phosphorylation levels of both CheA and CheY, and acetate repressed this stimulation. These observations suggest that CheY phosphorylation and acetylation are linked and co-regulated. We propose that the physiological role of these mutual effects is at two levels: linking chemotaxis to the metabolic state of the cell, and serving as a tuning mechanism that compensates for cell-to-cell variations in the concentrations of CheA and CheZ.
J Mol Biol 2004 Sep 10
PMID:Co-regulation of acetylation and phosphorylation of CheY, a response regulator in chemotaxis of Escherichia coli. 1532 41

Acetylation of CheY, the excitatory response regulator of bacterial chemotaxis, by the enzyme acetyl-CoA synthetase (Acs) is involved in Escherichia coli chemotaxis, but its function is obscure. Here, we overproduced Acs from E.coli, purified it in quantities sufficient for biochemical work, and characterized both the enzyme and the CheY acetylation reaction that it catalyzes. Such characterization is essential for revealing the function of CheY acetylation in chemotaxis. The enzyme exhibited characteristics typical of prokaryotic Acs enzymes, and it could use either acetate or AcCoA as an acetyl donor for CheY acetylation. The Acs-catalyzed acetylation of CheY was reversible, an essential property for a regulatory process, and cooperative (Hill coefficient approximately 3). By Western blotting with specific anti-acetyl-lysine antibody we demonstrated that Acs undergoes autoacetylation, that CheY is acetylated to a small extent when isolated, and that the extent is elevated following in vitro acetylation. Exposing the intact protein to matrix-assisted laser desorption ionization time-of-flight mass spectrometry and electro-spray mass spectrometry, we found that, in most cases, purified CheY is a mixture of species having zero to six acetyl groups per molecule, with non-acetylated CheY being the most abundant species. By proteolytic in-gel digestion of non-treated CheY followed by peptide fingerprinting, precursor ion scan, and tandem mass spectrometry, we found that the acetylation sites of CheY are clustered at the C terminus of the protein, with lysine residues 91, 92, 109, 119, 122 and 126 being the main acetylation sites. Following in vitro acetylation, the main change that seemed to occur was an incremental increase in the extent of acetylation of the same lysine residues. Thus, CheY is similar to many eukaryotic proteins involved in signaling, which undergo both phosphorylation and multiple acetylation, and in which the acetylation sites are restricted to a particular region.
J Mol Biol 2004 Sep 10
PMID:Acetylation of the chemotaxis response regulator CheY by acetyl-CoA synthetase purified from Escherichia coli. 1532 42

Accurate and rapid diagnostic tests can help identify high-risk patients with ACS among those presenting to the emergency department with chest pain. Such tests can also differentiate low-risk patients with chest pain who are suitable for early emergency department discharge. In this article, Drs Amsterdam and Deedwania elucidate the varieties of ACS, their pathophysiology, and the methods used for diagnosis. The authors also explore the potential of point-of-care testing for cardiac injury markers in the timely and accurate identification of ACS.
Postgrad Med 2005 Sep
PMID:Bedside evaluation of cardiac markers. Point-of-care testing can differentiate acute coronary syndromes. 1620 4

NSTE-ACS is a complex clinical event characterized by a variable degree of myocardial ischemia and triggered, in most patients, by a rupture of a vulnerable plaque that leads to acute intraluminal nonocclusive thrombosis. Traditionally, acute management strategies for NSTE-ACS have been aimed at identification of vascular areas with discrete atheroma and revascularization of the affected myocardium. Studies that have evaluated invasive strategies in NSTE-ACS suggest that the rates of hard clinical events are similar for both intensive medical treatment and early invasive management strategies. As shown recently in the Cooperative Cardiovascular Project study, intensive therapy with beta-blockers appears to be a viable management option that has comparable outcomes in most patients with NSTE-ACS. Although several different treatment strategies have been advocated in the management of NSTE-ACS, the available evidence-based information does not fully support some of these traditional approaches. Future prospective, well-controlled trials are needed to fully ascertain the role of invasive and other medical management strategies in patients with NSTE-ACS. Long-term aggressive management of established risk factors for CAD is unquestionably the most prudent and cost-effective therapeutic approach in the long-term management in patients recovering from NSTE-ACS.
Postgrad Med 2005 Sep
PMID:Treating non-ST-segment elevation ACS. Pros and cons of current strategies. 1620 5


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