PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 32845283-2 2020 Objective: To test the efficacy of the angiotensin receptor blocker telmisartan in slowing AAA growth in the Telmisartan in the Management of Abdominal Aortic Aneurysm (TEDY) trial. Telmisartan 68-79 AAA1 Homo sapiens 91-94 2581245-4 1985 At the 3" end of the insert a poly(A) addition signal A-A-T-A-A-A and part of the poly(A) tail of the messenger RNA were found. Poly A 30-36 AAA1 Homo sapiens 60-65 2581245-4 1985 At the 3" end of the insert a poly(A) addition signal A-A-T-A-A-A and part of the poly(A) tail of the messenger RNA were found. Poly A 30-37 AAA1 Homo sapiens 60-65 6519153-8 1984 Thus, it has been demonstrated that the AAA/AA ratio is an indicator of the acetylation phenotype, as it is closely correlated with that determined by dapsone (r = 0.895, p less than 0.0005). Dapsone 151-158 AAA1 Homo sapiens 40-46 6872343-7 1983 The other difference between AAA1 and AAA2 might stand in their specificity for the haptenic and structural determinants present in the glutaraldehyde-treated albumin. Glutaral 136-150 AAA1 Homo sapiens 29-33 33493273-6 2021 We designed, built, and characterized quantitatively a benchtop flow-loop using a deformable AAA silicone phantom representative of a patient-specific geometry. Silicones 97-105 AAA1 Homo sapiens 93-96 33332489-8 2021 We implemented all-atom molecular dynamics simulations and hybrid quantum-mechanics/molecular-mechanics simulations to explore the ATP hydrolysis mechanisms at the primary ATPase site (AAA1) of dynein. Adenosine Triphosphate 131-134 AAA1 Homo sapiens 185-189 33332489-10 2021 Here we explored the conformational changes upon binding of ATP at AAA1, nucleotide state-dependent regulation of the mechanochemical cycle, and inter-head coordination by inter-head tension. Adenosine Triphosphate 60-63 AAA1 Homo sapiens 67-71 2696647-8 1989 Male patients with AAA or dilated aortas were significantly heavier, with a lower ankle arm index and higher serum cholesterol values than patients without AAA or aortic dilatation. Cholesterol 115-126 AAA1 Homo sapiens 19-22 33780963-6 2021 The increase in luminal area preceded the increase in AAA diameter and was characterized by an overall deceleration in recirculation flow velocity with a coinciding increase in flow velocity penetrating the ILT. Phenobarbital 16-23 AAA1 Homo sapiens 54-57 32593727-4 2020 In the present study, we aimed to determine the global DNA methylation, homocysteine levels and their association with AAA and its growth. Homocysteine 72-84 AAA1 Homo sapiens 119-122 32593727-6 2020 We found significantly higher global DNA methylation (p < .001) and homocysteine levels (p < .001) in men with AAA compared to those without AAA, and direct linear associations with baseline aortic diameter. Homocysteine 68-80 AAA1 Homo sapiens 111-114 32593727-9 2020 We found that global DNA methylation and homocysteine levels are higher in men with AAA but are not associated with AAA growth. Homocysteine 41-53 AAA1 Homo sapiens 84-87 32845283-3 2020 Design, Setting, and Participants: A randomized, double-blind, placebo-controlled trial recruited participants between September 6, 2011, and October 5, 2016, to evaluate the efficacy of telmisartan treatment in patients with AAA. Telmisartan 187-198 AAA1 Homo sapiens 226-229 30936409-1 2019 OBJECTIVE: To assess the association of metformin prescription with the risk of aortic aneurysm, aortic aneurysm events and the enlargement of abdominal aortic aneurysm (AAA). Metformin 40-49 AAA1 Homo sapiens 170-173 33230227-6 2020 However, when AAA4 is bound to ATP, the gating of AAA1 by AAA3 prevails and dynein motion can occur. Adenosine Triphosphate 31-34 AAA1 Homo sapiens 50-54 32187752-7 2020 Currently, the most promising potential drug candidate to slow AAA growth is metformin, and RCTs to verify or reject this hypothesis are warranted. Metformin 77-86 AAA1 Homo sapiens 63-66 32410576-5 2020 CASE PRESENTATION: A 77-year-old woman on warfarin with a known AAA presented to our ED with 2 days of epigastric abdominal pain. Warfarin 42-50 AAA1 Homo sapiens 64-67 32063115-9 2020 Positive log-linear associations with AAA for women and men were also observed for usual body mass index, usual systolic blood pressure, height, usual low-density lipoprotein cholesterol, and usual triglycerides. Cholesterol 175-186 AAA1 Homo sapiens 38-41 32063115-9 2020 Positive log-linear associations with AAA for women and men were also observed for usual body mass index, usual systolic blood pressure, height, usual low-density lipoprotein cholesterol, and usual triglycerides. Triglycerides 198-211 AAA1 Homo sapiens 38-41 31872818-3 2020 Herein, molecular dynamics simulations of a dynein motor disclosed that two water molecules are present close to the gamma-phosphate of ATP and Glu1742 at the AAA1 site of dynein. Water 76-81 AAA1 Homo sapiens 159-163 31872818-3 2020 Herein, molecular dynamics simulations of a dynein motor disclosed that two water molecules are present close to the gamma-phosphate of ATP and Glu1742 at the AAA1 site of dynein. gamma-phosphate 117-132 AAA1 Homo sapiens 159-163 31872818-3 2020 Herein, molecular dynamics simulations of a dynein motor disclosed that two water molecules are present close to the gamma-phosphate of ATP and Glu1742 at the AAA1 site of dynein. Adenosine Triphosphate 136-139 AAA1 Homo sapiens 159-163 31896597-10 2020 Taken together, these data indicated the crucial functions of TER94 at multiple steps of the baculovirus life cycle, including genome replication, BV formation, and ODV morphogenesis.IMPORTANCE TER94 constitutes an important AAA+ ATPase that associates with diverse cellular processes, including protein quality control, membrane fusion of the Golgi apparatus and endoplasmic reticulum network, nuclear envelope reformation, and DNA replication. ter94 62-67 AAA1 Homo sapiens 225-236 31891071-2 2019 Among the six AAA+ domains, AAA1 is the primary ATPase site where a single ATP hydrolysis generates a single step. Adenosine Triphosphate 48-51 AAA1 Homo sapiens 28-32 31891071-6 2019 ATP binding to the AAA1 domain creates a cascade of conformational changes through the other domains of the ring, which leads to the pre-power stroke formation. Adenosine Triphosphate 0-3 AAA1 Homo sapiens 19-23 31526123-12 2019 In patients with complex AAA, 4 strokes occurred among rivaroxaban-assigned patients and 4 strokes among aspirin-assigned patients. Rivaroxaban 55-66 AAA1 Homo sapiens 25-28 31526123-12 2019 In patients with complex AAA, 4 strokes occurred among rivaroxaban-assigned patients and 4 strokes among aspirin-assigned patients. Aspirin 105-112 AAA1 Homo sapiens 25-28 30936409-9 2019 We found that metformin prescription could significantly limit the enlargement of aortic aneurysm (weighted mean difference: -0.83 mm/year, 95% CI -1.38 to -0.28, I2=89.6%) among patients with AAA. Metformin 14-23 AAA1 Homo sapiens 193-196 30936409-11 2019 CONCLUSIONS: According to the available epidemiological evidence, metformin prescription could limit the expansion of AAA among patients with this disease, and may be involved with a lower incidence of aortic aneurysm and aortic aneurysm events. Metformin 66-75 AAA1 Homo sapiens 118-121 30936409-12 2019 Randomised controlled trials are needed to confirm whether metformin could reduce the enlargement of AAA in patients with or without diabetes. Metformin 59-68 AAA1 Homo sapiens 101-104 30270176-3 2018 Binding of ATP closes the cleft between the AAA1 and AAA2 domains, triggering conformational changes in the rest of the motor domain, thus forming the pre-power stroke state. Adenosine Triphosphate 11-14 AAA1 Homo sapiens 44-48 31300976-9 2019 Comparing bond scissions at the amide linkage between Cit-Zzz (citrulline followed by a specified residue) to Aaa1-Aaa2 (Aaa can be any residue except Cit), 5 Cit-Zzz cleavages were significantly (CL = 95.0%) more frequent in > 85% of the cases in terms of relative sequential base beak occurrence. Amides 32-37 AAA1 Homo sapiens 110-114 31300976-9 2019 Comparing bond scissions at the amide linkage between Cit-Zzz (citrulline followed by a specified residue) to Aaa1-Aaa2 (Aaa can be any residue except Cit), 5 Cit-Zzz cleavages were significantly (CL = 95.0%) more frequent in > 85% of the cases in terms of relative sequential base beak occurrence. Amides 32-37 AAA1 Homo sapiens 110-113 31239294-7 2019 The quantification of oxysterols, performed by liquid chromatography-(atmospheric pressure chemical ionization (APCI))-mass spectrometry, showed that levels of 7-KC were significantly higher while those of 7alpha-hydroxycholesterol (HC), 24-HC and 27-HC were lower in AAA patients compared with healthy donors. Oxysterols 22-32 AAA1 Homo sapiens 268-271 29628493-7 2018 Therefore, we focused on the diet-induced abnormal triglyceride metabolism, which has the potential to drive AAA development. Triglycerides 51-63 AAA1 Homo sapiens 109-112 30300293-1 2018 BACKGROUND: Some evidence suggests that off-label use of mirtazapine (15 mg) is effective in treatment of acute antipsychotic-associated akathisia (AAA). Mirtazapine 57-68 AAA1 Homo sapiens 106-152 30300293-2 2018 We analyzed whether a lower dose of mirtazapine (7.5 mg) maintained its antiakathisia properties while exhibiting better tolerability in patients with schizophrenia and mood disorders who developed acute AAA. Mirtazapine 36-47 AAA1 Homo sapiens 204-207 30300293-9 2018 CONCLUSIONS: A large-scale controlled evaluation is warranted to substantiate clinical utility of off-label use of mirtazapine (7.5 mg) for patients with AAA. Mirtazapine 115-126 AAA1 Homo sapiens 154-157 30248405-9 2018 Here we describe recent data indicating that montelukast may be used for prevention and treatment of AAA, thus representing a promising pharmacological tool for a deadly vascular disease with significant socio-economic impact. montelukast 45-56 AAA1 Homo sapiens 101-104 29628493-8 2018 In this study, we have evaluated the effects of a high-sucrose diet on the development of AAA in a vascular hypoperfusion-induced animal model. Sucrose 55-62 AAA1 Homo sapiens 90-93 29037509-0 2018 Structure determination of disease associated peak AAA from l-Tryptophan implicated in the eosinophilia-myalgia syndrome. Tryptophan 60-72 AAA1 Homo sapiens 51-54 29238828-9 2018 This approach was applied to a silicone phantom model of an AAA reconstructed from a patient"s computed tomography-scan examination. Silicones 31-39 AAA1 Homo sapiens 60-63 29432192-3 2018 Here we show that antagonism of the CysLT1 receptor by montelukast, an established antiasthma drug, protects against a strong aorta dilatation (>50% increase = aneurysm) in a mouse model of CaCl2-induced AAA at a dose comparable to human medical practice. montelukast 55-66 AAA1 Homo sapiens 207-210 29432192-7 2018 Moreover, montelukast reduced the incidence of aortic rupture and attenuated the AAA development in two additional independent models, i.e., angiotensin II- and porcine pancreatic elastase-induced AAA, respectively. montelukast 10-21 AAA1 Homo sapiens 81-84 29432192-7 2018 Moreover, montelukast reduced the incidence of aortic rupture and attenuated the AAA development in two additional independent models, i.e., angiotensin II- and porcine pancreatic elastase-induced AAA, respectively. montelukast 10-21 AAA1 Homo sapiens 197-200 29432192-8 2018 Our results indicate that cys-LTs are involved in the pathogenesis of AAA and that antagonism of the CysLT1 receptor is a promising strategy for preventive and therapeutic treatment of this clinically silent and highly lethal disease. Cysteine 26-29 AAA1 Homo sapiens 70-73 29037509-7 2018 By comparing the LC-MS and LC-MS-MS retention times and spectra with authentic synthetic standards, Peak AAA1 was identified as the intermolecular condensation product of L-Trp with anteiso 7-methylnonanoic acid, to afford (S)-2-amino-3-(2-((S,E)-7-methylnon-1-en-1-yl)-1H-indol-3-yl)propanoic acid. (s)-2-amino-3-(2-((s,e)-7-methylnon-1-en-1-yl)-1h-indol-3-yl)propanoic acid 223-298 AAA1 Homo sapiens 105-109 29037509-6 2018 Peak AAA1 and Peak AAA2 differed in LC retention times, and were determined by accurate mass-LC-MS to both have a protonated molecular ion (MH+) of mass 343.239Da (Da), corresponding to a molecular formula of C21H30N2O2, and possessing eight degrees of unsaturation (DoU) for the non-protonated molecule. c21h30n2o2 209-219 AAA1 Homo sapiens 5-9 29037509-7 2018 By comparing the LC-MS and LC-MS-MS retention times and spectra with authentic synthetic standards, Peak AAA1 was identified as the intermolecular condensation product of L-Trp with anteiso 7-methylnonanoic acid, to afford (S)-2-amino-3-(2-((S,E)-7-methylnon-1-en-1-yl)-1H-indol-3-yl)propanoic acid. Tryptophan 171-176 AAA1 Homo sapiens 105-109 29037509-7 2018 By comparing the LC-MS and LC-MS-MS retention times and spectra with authentic synthetic standards, Peak AAA1 was identified as the intermolecular condensation product of L-Trp with anteiso 7-methylnonanoic acid, to afford (S)-2-amino-3-(2-((S,E)-7-methylnon-1-en-1-yl)-1H-indol-3-yl)propanoic acid. anteiso 7-methylnonanoic acid 182-211 AAA1 Homo sapiens 105-109 30317710-7 2018 Patients with AAA were significantly more medicated with acetylsalicylic acid and had more aortic thrombi (P=0,031 and P=0,002, respectively). Aspirin 57-77 AAA1 Homo sapiens 14-17 28288701-4 2017 Recent studies using rodent models of AAA suggest that long chain omega-3 polyunsaturated fatty acids (LC n-3 PUFAs) and their metabolites can moderate inflammation and oxidative stress perpetuated by infiltrating macrophages and intervene in the destruction of medial elastin. omega-3 polyunsaturated fatty acids 66-101 AAA1 Homo sapiens 38-41 28588751-6 2017 The baseline branched chain amino acids/aromatic amino acids (BCAA/AAA) ratio was higher in the healthy persons and remained stable-but it decreased significantly after the meal in the cirrhotic group. Amino Acids, Branched-Chain 13-39 AAA1 Homo sapiens 67-70 28588751-6 2017 The baseline branched chain amino acids/aromatic amino acids (BCAA/AAA) ratio was higher in the healthy persons and remained stable-but it decreased significantly after the meal in the cirrhotic group. Amino Acids, Aromatic 40-60 AAA1 Homo sapiens 67-70 28588751-7 2017 After the high protein meal there was a marked increase in the levels of most amino acids, but only small changes occurred in the levels of taurine, citrulline, cysteine and histidine.The BCAA/AAA ratio was significantly higher 180 and 240 min after the meal. Cysteine 161-169 AAA1 Homo sapiens 193-196 28287739-8 2017 Patterns of metabolite variation associated with AAA relate to carbohydrate and lipid metabolism. Carbohydrates 63-75 AAA1 Homo sapiens 49-52 28237648-17 2017 The presence of an AAA was significantly correlated with male sex (P < 0.001), advanced age (P = 0.01), smoking (P < 0.001), alcohol consumption (P < 0.01), and the presence of pulmonary disease (P = 0.01). Alcohols 131-138 AAA1 Homo sapiens 19-22 28237648-20 2017 Male sex, old age, smoking, alcohol use, and pulmonary disease are possible risk factors for AAA in the general Korean population. Alcohols 28-35 AAA1 Homo sapiens 93-96 27886288-1 2016 Dyneins, a class of motor proteins consisting of six AAA+ modules (AAA1-AAA6), convert chemical energy derived from the hydrolysis of ATP into mechanical energy to walk along the microtubule track towards its minus end while accomplishing various cellular tasks including the transportation of various intracellular cargos. Adenosine Triphosphate 134-137 AAA1 Homo sapiens 67-76 28079254-17 2017 A subgroup of 227 participants with AAA received either metoprolol (N = 111) or placebo (N = 116). Metoprolol 56-66 AAA1 Homo sapiens 36-39 27886288-2 2016 In a full mechanochemical cycle, dynein goes through ATP binding induced open to closed state transition of AAA1, hydrolysis of that ATP and closed to open state transition induced by the release of hydrolysed products along with linker remodelling in different nucleotide states. Adenosine Triphosphate 53-56 AAA1 Homo sapiens 108-112 27740761-1 2016 Arginine finger is a highly conserved and essential residue in many GTPase and AAA+ ATPase enzymes that completes the active site from a distinct protomer, forming contacts with the gamma-phosphate of the nucleotide. gamma-phosphate 182-197 AAA1 Homo sapiens 79-90 26497651-4 2016 Hyperammonemia combined with a decrease on the BCA/AAA ratio induces alterations of energetic metabolism and the formation of free radicals in the CNS. Free Radicals 126-139 AAA1 Homo sapiens 51-54 27634835-4 2016 APPROACH AND RESULTS: In angiotensin II-induced ApoE-/- mouse and CaCl2-induced C57BL/6J mouse model of AAA, IMD1-53 significantly reduced the incidence of AAA and maximal aortic diameter. Calcium Chloride 66-71 AAA1 Homo sapiens 104-107 27634835-4 2016 APPROACH AND RESULTS: In angiotensin II-induced ApoE-/- mouse and CaCl2-induced C57BL/6J mouse model of AAA, IMD1-53 significantly reduced the incidence of AAA and maximal aortic diameter. Calcium Chloride 66-71 AAA1 Homo sapiens 156-159 27499372-7 2016 In human AAA samples, the amount of triglyceride in the adventitia was correlated with the diameter of the AAA. Triglycerides 36-48 AAA1 Homo sapiens 9-12 27703410-3 2016 AAA+ proteins are defined by conserved modules that precisely position the active site elements of two adjacent subunits to catalyze ATP hydrolysis. Adenosine Triphosphate 133-136 AAA1 Homo sapiens 0-3 27499372-7 2016 In human AAA samples, the amount of triglyceride in the adventitia was correlated with the diameter of the AAA. Triglycerides 36-48 AAA1 Homo sapiens 107-110 25637566-8 2015 The elevated levels of cadmium in the walls of AAA coexisting with IAAs may suggest an impact of the accumulation of this trace element on the greater damage of the iliac artery wall. Cadmium 23-30 AAA1 Homo sapiens 47-50 27334455-5 2016 In this work, we built two models named "the ADP model" and "the ATP model", where ADP and ATP are bound to AAA1 in the AAA(+) ring, respectively, to observe the initial procedure of the structural change from the unprimed to the primed state. Adenosine Triphosphate 65-68 AAA1 Homo sapiens 108-112 27334455-5 2016 In this work, we built two models named "the ADP model" and "the ATP model", where ADP and ATP are bound to AAA1 in the AAA(+) ring, respectively, to observe the initial procedure of the structural change from the unprimed to the primed state. Adenosine Diphosphate 83-86 AAA1 Homo sapiens 108-112 27334455-5 2016 In this work, we built two models named "the ADP model" and "the ATP model", where ADP and ATP are bound to AAA1 in the AAA(+) ring, respectively, to observe the initial procedure of the structural change from the unprimed to the primed state. Adenosine Triphosphate 91-94 AAA1 Homo sapiens 108-112 26496478-5 2015 We used four methods to test and verify the performance of this level-2 PPI network: cross validation, human AAA mRNA chip array comparison, literature mining, and verification in a mouse CaPO4 AAA model. capo4 188-193 AAA1 Homo sapiens 194-197 26639068-4 2016 The aim of this study was to evaluate the usefulness of calcium accumulation in the AAA for predicting its expansion rate. Calcium 56-63 AAA1 Homo sapiens 84-87 26454172-2 2015 Structures of AAA were determined in its native form and in complex with the analgesic acetanilide, p-acetaminophenol, at 1.70 A and 1.73 A resolutions, respectively. acetanilide 87-98 AAA1 Homo sapiens 14-17 26454172-2 2015 Structures of AAA were determined in its native form and in complex with the analgesic acetanilide, p-acetaminophenol, at 1.70 A and 1.73 A resolutions, respectively. 4-amino-N-acetyl-N-methylaniline 100-117 AAA1 Homo sapiens 14-17 26454172-9 2015 The optimum activity of AAA at pH > 10 suggests that the reaction mechanism employs Lys(84) as the catalytic base to polarize the Ser(187) nucleophile in the catalytic triad. Lysine 87-90 AAA1 Homo sapiens 24-27 26454172-9 2015 The optimum activity of AAA at pH > 10 suggests that the reaction mechanism employs Lys(84) as the catalytic base to polarize the Ser(187) nucleophile in the catalytic triad. Serine 133-136 AAA1 Homo sapiens 24-27 25941405-3 2015 The main site of ATP hydrolysis, AAA1, is the only site considered by most dynein motility models. Adenosine Triphosphate 17-20 AAA1 Homo sapiens 33-37 24732583-1 2015 The aim of this paper was to summarize the present evidence for an association between circulating total homocysteine (tHcy) levels and abdominal aortic aneurysm (AAA) presence, we performed a meta-analysis. Homocysteine 105-117 AAA1 Homo sapiens 163-166 24732583-1 2015 The aim of this paper was to summarize the present evidence for an association between circulating total homocysteine (tHcy) levels and abdominal aortic aneurysm (AAA) presence, we performed a meta-analysis. thcy 119-123 AAA1 Homo sapiens 163-166 24732583-4 2015 Eligible studies were case-control or population-screening studies reporting circulating tHcy levels in cases with AAA and subjects without AAA. thcy 89-93 AAA1 Homo sapiens 115-118 24732583-8 2015 A pooled analysis demonstrated significantly greater circulating tHcy levels in the AAA than control group (SMD, 0.58; 95% CI, 0.36 to 0.79; P<0.00001). thcy 65-69 AAA1 Homo sapiens 84-87 24732583-10 2015 In conclusion, greater circulating tHcy levels are associated with AAA presence. thcy 35-39 AAA1 Homo sapiens 67-70 25941405-9 2015 Using nucleotide binding and hydrolysis mutants, we show that, although ATP exerts its effects via binding AAA1, ADP effects are mediated by AAA3. Adenosine Triphosphate 72-75 AAA1 Homo sapiens 107-111 25941405-9 2015 Using nucleotide binding and hydrolysis mutants, we show that, although ATP exerts its effects via binding AAA1, ADP effects are mediated by AAA3. Adenosine Diphosphate 113-116 AAA1 Homo sapiens 107-111 25941405-11 2015 When tension is absent or applied via dynein"s C terminus, ATP binding to AAA1 induces MT release only if AAA3 is in the posthydrolysis state. Adenosine Triphosphate 59-62 AAA1 Homo sapiens 74-78 24449038-15 2014 A subgroup of 227 patients with AAA received either metoprolol (N = 111) or placebo (N = 116). Metoprolol 52-62 AAA1 Homo sapiens 32-35 24651519-9 2014 Intraoperative indocyanine green fluorescence lymphography revealed lymph stasis in intima/medial in AAA. Indocyanine Green 15-32 AAA1 Homo sapiens 101-104 25517227-2 2015 Uptake of 18-fluorodeoxyglucose (FDG) detected by positron emission tomography (PET) is observed in the wall of 12% of AAA (A+), with most of them being symptomatic. 18-fluorodeoxyglucose 10-31 AAA1 Homo sapiens 119-122 25517227-2 2015 Uptake of 18-fluorodeoxyglucose (FDG) detected by positron emission tomography (PET) is observed in the wall of 12% of AAA (A+), with most of them being symptomatic. fluorescein-digalactoside 33-36 AAA1 Homo sapiens 119-122 25036037-1 2014 BACKGROUND: Salt intake has been implicated in the pathogenesis of abdominal aortic aneurysm (AAA) through studies in rodent models but not previously studied in humans. Salts 12-16 AAA1 Homo sapiens 94-97 25036037-2 2014 The aim of this study was to examine the association between reported addition of salt to food and the prevalence of AAA. Salts 82-86 AAA1 Homo sapiens 117-120 25036037-5 2014 RESULTS: The prevalence of AAA was 6.9, 8.5 and 8.6% in men who reported adding salt to food never, sometimes and always, respectively, p = 0.005. Salts 80-84 AAA1 Homo sapiens 27-30 25036037-6 2014 Addition of salt to food sometimes (odds ratio [OR]: 1.22, 95% confidence interval [CI]: 1.03-1.44) or always (OR: 1.23, 95% CI 1.04-1.47) was independently associated with AAA after adjustment for other risk factors including age, waist-hip ratio, blood pressure, history of hypertension, high cholesterol, angina, diabetes, myocardial infarction and stroke. Salts 12-16 AAA1 Homo sapiens 173-176 25036037-9 2014 CONCLUSION: Reported salt intake is associated with AAA in older men. Salts 21-25 AAA1 Homo sapiens 52-55 25036037-10 2014 Additional studies are needed to determine whether reducing salt intake would protect against AAA. Salts 60-64 AAA1 Homo sapiens 94-97 24365123-13 2014 There was a significantly high frequency of the rs10757278 GG genotype in AAA patients with high serum total homocysteine compared with those control subjects with high serum total homocysteine (OR, 2.71; 95% CI, 1.12-6.58; P = .03) indicating that the genotype GG of rs10757278 might interact with the homocysteine biological pathway to stimulate the presence of AAA. Homocysteine 109-121 AAA1 Homo sapiens 74-77 24365123-13 2014 There was a significantly high frequency of the rs10757278 GG genotype in AAA patients with high serum total homocysteine compared with those control subjects with high serum total homocysteine (OR, 2.71; 95% CI, 1.12-6.58; P = .03) indicating that the genotype GG of rs10757278 might interact with the homocysteine biological pathway to stimulate the presence of AAA. Homocysteine 109-121 AAA1 Homo sapiens 364-367 24365123-13 2014 There was a significantly high frequency of the rs10757278 GG genotype in AAA patients with high serum total homocysteine compared with those control subjects with high serum total homocysteine (OR, 2.71; 95% CI, 1.12-6.58; P = .03) indicating that the genotype GG of rs10757278 might interact with the homocysteine biological pathway to stimulate the presence of AAA. Homocysteine 181-193 AAA1 Homo sapiens 74-77 24365123-13 2014 There was a significantly high frequency of the rs10757278 GG genotype in AAA patients with high serum total homocysteine compared with those control subjects with high serum total homocysteine (OR, 2.71; 95% CI, 1.12-6.58; P = .03) indicating that the genotype GG of rs10757278 might interact with the homocysteine biological pathway to stimulate the presence of AAA. Homocysteine 181-193 AAA1 Homo sapiens 74-77 24448739-8 2014 Three diacylglycerols and 7 triacylglycerols were associated with AAA. Diglycerides 6-21 AAA1 Homo sapiens 66-69 24448739-8 2014 Three diacylglycerols and 7 triacylglycerols were associated with AAA. Triglycerides 28-44 AAA1 Homo sapiens 66-69 24448739-10 2014 CONCLUSIONS: A group of linoleic acid containing triacylglycerols and diacylglycerols were significantly associated with AAA presence. Linoleic Acid 24-37 AAA1 Homo sapiens 121-124 24448739-10 2014 CONCLUSIONS: A group of linoleic acid containing triacylglycerols and diacylglycerols were significantly associated with AAA presence. Triglycerides 49-65 AAA1 Homo sapiens 121-124 24448739-10 2014 CONCLUSIONS: A group of linoleic acid containing triacylglycerols and diacylglycerols were significantly associated with AAA presence. Diglycerides 70-85 AAA1 Homo sapiens 121-124 23776210-4 2013 We demonstrate that MuB is an ATPase associated with diverse cellular activities (AAA+ ATPase) and forms ATP-dependent filaments with or without DNA. Adenosine Triphosphate 30-33 AAA1 Homo sapiens 82-93 24091093-10 2013 Multivariate analysis showed that larger AAA diameter (odds ratio [OR]: 1.048/mm increase; 95% confidence interval [CI]: 1.042-1.082; p < .001) and a higher AAC-8 score (OR: 1.34/point increase; 95% CI: 1.19-1.53; p < .001) were significantly associated with development into a sAAA or rAAA. saaa 284-288 AAA1 Homo sapiens 41-44 24091093-10 2013 Multivariate analysis showed that larger AAA diameter (odds ratio [OR]: 1.048/mm increase; 95% confidence interval [CI]: 1.042-1.082; p < .001) and a higher AAC-8 score (OR: 1.34/point increase; 95% CI: 1.19-1.53; p < .001) were significantly associated with development into a sAAA or rAAA. raaa 292-296 AAA1 Homo sapiens 41-44 23047410-3 2012 We report a case of a 78-year-old, ASA IV patient suffering from acute cholecystitis and concomitant (62 mm) AAA. Aspirin 35-38 AAA1 Homo sapiens 109-112 23602862-1 2013 OBJECTIVE: This study aims to investigate the association between plasma 25-hydroxyvitamin D (25(OH)D) concentrations with the presence of abdominal aortic aneurysm (AAA) and aortic diameter. 25-hydroxyvitamin D 73-92 AAA1 Homo sapiens 166-169 23602862-8 2013 CONCLUSIONS: Low vitamin D status is associated with the presence of larger AAA in older men, and there is a graded inverse relationship between 25(OH)D concentrations and AAA diameter. Vitamin D 17-26 AAA1 Homo sapiens 76-79 23711681-10 2013 CONCLUSION: The effects of atorvastatin seem to prevent the histopathological progression of AAA. Atorvastatin 27-39 AAA1 Homo sapiens 93-96 23044097-3 2013 One animal model of AAA involves peri-vascular application of calcium chloride (CaCl(2)) onto the infra-renal aorta of mice and rats to induce extracellular matrix remodelling. Calcium Chloride 62-78 AAA1 Homo sapiens 20-23 23044097-3 2013 One animal model of AAA involves peri-vascular application of calcium chloride (CaCl(2)) onto the infra-renal aorta of mice and rats to induce extracellular matrix remodelling. Calcium Chloride 80-87 AAA1 Homo sapiens 20-23 23044097-7 2013 CaCl(2)-induced AAA shows the following pathological characteristics typically found in human AAA: calcification, inflammatory cell infiltration, oxidative stress, neovascularisation, elastin degradation and vascular smooth muscle cell apoptosis. Calcium Chloride 0-7 AAA1 Homo sapiens 16-19 23044097-7 2013 CaCl(2)-induced AAA shows the following pathological characteristics typically found in human AAA: calcification, inflammatory cell infiltration, oxidative stress, neovascularisation, elastin degradation and vascular smooth muscle cell apoptosis. Calcium Chloride 0-7 AAA1 Homo sapiens 94-97 23044097-8 2013 A number of mechanisms involved in CaCl(2)-induced AAA have been identified which may be relevant to the pathogenesis of human AAA. Calcium Chloride 35-42 AAA1 Homo sapiens 51-54 23044097-8 2013 A number of mechanisms involved in CaCl(2)-induced AAA have been identified which may be relevant to the pathogenesis of human AAA. Calcium Chloride 35-42 AAA1 Homo sapiens 127-130 23044097-10 2013 CaCl(2)-induced AAA does not display aortic thrombus, atherosclerosis and rupture which are classical features of human AAA. Calcium Chloride 0-7 AAA1 Homo sapiens 16-19 23044097-11 2013 Advantages of the CaCl(2)-induced AAA technique include (1) it can be applied to wild type mice making assessment of transgenic rodent models more straight forward and rapid; and (2) CaCl(2)-induced AAAs are usually developed in the infra-renal abdominal aorta, which is the most common location of human AAA. Calcium Chloride 18-25 AAA1 Homo sapiens 34-37 23044097-11 2013 Advantages of the CaCl(2)-induced AAA technique include (1) it can be applied to wild type mice making assessment of transgenic rodent models more straight forward and rapid; and (2) CaCl(2)-induced AAAs are usually developed in the infra-renal abdominal aorta, which is the most common location of human AAA. Calcium Chloride 18-25 AAA1 Homo sapiens 199-202 23044097-11 2013 Advantages of the CaCl(2)-induced AAA technique include (1) it can be applied to wild type mice making assessment of transgenic rodent models more straight forward and rapid; and (2) CaCl(2)-induced AAAs are usually developed in the infra-renal abdominal aorta, which is the most common location of human AAA. Calcium Chloride 183-190 AAA1 Homo sapiens 34-37 23044097-11 2013 Advantages of the CaCl(2)-induced AAA technique include (1) it can be applied to wild type mice making assessment of transgenic rodent models more straight forward and rapid; and (2) CaCl(2)-induced AAAs are usually developed in the infra-renal abdominal aorta, which is the most common location of human AAA. Calcium Chloride 183-190 AAA1 Homo sapiens 199-202 23044097-12 2013 Currently findings obtained from the CaCl(2)-induced AAA model or other animal models of AAA have not been translated into the human situation. Calcium Chloride 37-44 AAA1 Homo sapiens 53-56 22854530-6 2012 Randomized trials of doxycycline, roxithromycin, and propranolol in patients with small AAA have been published. Doxycycline 21-32 AAA1 Homo sapiens 88-91 22854530-6 2012 Randomized trials of doxycycline, roxithromycin, and propranolol in patients with small AAA have been published. Roxithromycin 34-47 AAA1 Homo sapiens 88-91 22854530-6 2012 Randomized trials of doxycycline, roxithromycin, and propranolol in patients with small AAA have been published. Propranolol 53-64 AAA1 Homo sapiens 88-91 22854530-7 2012 The results of the doxycycline and roxithromycin trials suggest that both medications can limit AAA expansion, especially during the first year of treatment. Doxycycline 19-30 AAA1 Homo sapiens 96-99 22854530-7 2012 The results of the doxycycline and roxithromycin trials suggest that both medications can limit AAA expansion, especially during the first year of treatment. Roxithromycin 35-48 AAA1 Homo sapiens 96-99 22854530-9 2012 In other studies, statins and indomethacin have also been shown to limit AAA expansion. Indomethacin 30-42 AAA1 Homo sapiens 73-76 22519354-3 2012 First, we have used normal mode analysis to identify a single normal mode that captures the coupled motions of AAA1-AAA2 closing and linker domain rotation, which enables the ATP-driven recovery stroke of dynein. Adenosine Triphosphate 175-178 AAA1 Homo sapiens 111-115 22543712-3 2012 Metabolic changes in AAA patients were mainly related to carbohydrate and lipid metabolism and many of these changes can be associated with a situation of insulin resistance (which can be related to metabolic syndrome) together with altered amino acid metabolism. Carbohydrates 57-69 AAA1 Homo sapiens 21-24 22384120-7 2012 Identified metabolites indicate a role for sphingolipids, lysophospholipids, cholesterol metabolites, and acylcarnitines in the development and progression of AAA. Sphingolipids 43-56 AAA1 Homo sapiens 159-162 21985917-11 2012 Although the lysine encoded by AAG was identical to the lysine encoded by AAA, it is not clear if they have functional differences due to the changing environmental conditions. Lysine 56-62 AAA1 Homo sapiens 74-77 22357537-8 2012 Similar results were seen in mice with AAA augmented by nicotine and in human aortic tissue samples from patients undergoing surgical repair of AAA (with more pronounced effects observed in smokers). Nicotine 56-64 AAA1 Homo sapiens 39-42 22425997-7 2012 Ciliobrevins therefore will be useful reagents for studying cellular processes that require this microtubule motor and may guide the development of additional AAA+ ATPase superfamily inhibitors. ciliobrevins 0-12 AAA1 Homo sapiens 159-170 21736903-1 2012 ClpXP is a AAA+ protease that uses the energy of ATP binding and hydrolysis to perform mechanical work during targeted protein degradation within cells. Adenosine Triphosphate 49-52 AAA1 Homo sapiens 11-14 22384120-7 2012 Identified metabolites indicate a role for sphingolipids, lysophospholipids, cholesterol metabolites, and acylcarnitines in the development and progression of AAA. Lysophospholipids 58-75 AAA1 Homo sapiens 159-162 22384120-7 2012 Identified metabolites indicate a role for sphingolipids, lysophospholipids, cholesterol metabolites, and acylcarnitines in the development and progression of AAA. Cholesterol 77-88 AAA1 Homo sapiens 159-162 22384120-8 2012 Moreover, guanidinosuccinic acid, which mimics nitric oxide in terms of its vasodilatory action, was found as a strong marker of large AAA. guanidinosuccinic acid 10-32 AAA1 Homo sapiens 135-138 22384120-8 2012 Moreover, guanidinosuccinic acid, which mimics nitric oxide in terms of its vasodilatory action, was found as a strong marker of large AAA. Nitric Oxide 47-59 AAA1 Homo sapiens 135-138 21621776-2 2011 As cholesterol crystals have also been found in the walls of patients with abdominal aortic aneurysms (AAA), it is possible that the NLRP3 inflammasome is involved in AAA and genetic variability within this protein complex could alter disease risk. Cholesterol 3-14 AAA1 Homo sapiens 103-106 21621776-2 2011 As cholesterol crystals have also been found in the walls of patients with abdominal aortic aneurysms (AAA), it is possible that the NLRP3 inflammasome is involved in AAA and genetic variability within this protein complex could alter disease risk. Cholesterol 3-14 AAA1 Homo sapiens 167-170 20887020-14 2010 The pulsatile AAA PHE FEM demonstrated a complex interstitial fluid velocity field the direction of which alternated in to and out of the luminal layer of the ILT. Phenylalanine 18-21 AAA1 Homo sapiens 14-17 21595625-6 2011 Animal studies of doxcycline for AAA provide significant evidence of a beneficial effect. doxcycline 18-28 AAA1 Homo sapiens 33-36 21595625-11 2011 The evidence for any beneficial effect of doxycycline as a treatment for AAA, therefore, remains weak. Doxycycline 42-53 AAA1 Homo sapiens 73-76 20521434-0 2010 AAA- a further step towards a moratorium for aspirin in the primary prevention. Aspirin 45-52 AAA1 Homo sapiens 0-3 19961937-8 2010 We propose that an altered occupancy of the different ATP binding sites (AAA1-4) acts as a modulator between processive and non-processive stepping. Adenosine Triphosphate 54-57 AAA1 Homo sapiens 73-79 20717088-12 2010 In conclusion, Eclipse AAA commissioned at standard SSD can be used to accurately predict dose distributions in water at extended SSD for 6 MV open beams. Water 112-117 AAA1 Homo sapiens 23-26 20061425-9 2010 Men with AAA had lower serum total and free testosterone (mean +/- sd 14.5 +/- 6.0 vs. 15.5 +/- 5.6 nmol/liter, P = 0.005 and 256 +/- 87 vs. 280 +/- 97 pmol/liter, P < 0.001, respectively) compared with men without. Testosterone 44-56 AAA1 Homo sapiens 9-12 20061425-11 2010 In multivariate analysis adjusting for potential confounders, free testosterone was negatively associated with AAA (odds ratio per 1 sd increase: 0.84, 95% confidence interval 0.72-0.98, P = 0.026). Testosterone 67-79 AAA1 Homo sapiens 111-114 20061425-14 2010 CONCLUSIONS: Lower free testosterone and higher LH levels are independently associated with AAA in older men. Testosterone 24-36 AAA1 Homo sapiens 92-95 18367268-2 2009 Patients with AAA had lower HDL-cholesterol (p<.0001), increased triglycerides (p=.0002) and smaller LDL size (p<.0001) as well as increased levels of total small, dense LDL (p=.0210) in relation to controls. Cholesterol 32-43 AAA1 Homo sapiens 14-17 20149231-1 2010 INTRODUCTION: Alterations in circulating large neutral amino acids (LNAAs), leading to a decrease in the plasma ratio between branched-chain and aromatic amino acids (BCAA/AAA ratio), may be involved in sepsis-associated encephalopathy. Amino Acids, Aromatic 145-165 AAA1 Homo sapiens 172-175 18367268-2 2009 Patients with AAA had lower HDL-cholesterol (p<.0001), increased triglycerides (p=.0002) and smaller LDL size (p<.0001) as well as increased levels of total small, dense LDL (p=.0210) in relation to controls. Triglycerides 68-81 AAA1 Homo sapiens 14-17 18855713-9 2008 While no medical treatment is yet approved, doxycycline (Doxy) has been shown to greatly reduce AAA growth in animal models and has been shown to slow growth in 1 small clinical trial. Doxycycline 44-55 AAA1 Homo sapiens 96-99 18855713-9 2008 While no medical treatment is yet approved, doxycycline (Doxy) has been shown to greatly reduce AAA growth in animal models and has been shown to slow growth in 1 small clinical trial. Doxycycline 57-61 AAA1 Homo sapiens 96-99 17242399-2 2007 Activators of the bacterial sigma(54)-RNAP are AAA+ proteins that couple ATP hydrolysis to restructure the sigma(54)-RNAP promoter complex. Adenosine Triphosphate 73-76 AAA1 Homo sapiens 47-50 17497968-4 2007 Our objective was to review the published work with regard to the role of homocysteine in the pathogenesis of AAA. Homocysteine 74-86 AAA1 Homo sapiens 110-113 17497968-7 2007 Several case-control studies report an association between increased levels of homocysteine and the presence of an AAA. Homocysteine 79-91 AAA1 Homo sapiens 115-118 17497968-9 2007 Although there is evidence for an association between homocysteine and AAA, it is not strong enough to conclude that it plays a causal role in the pathogenesis of AAA. Homocysteine 54-66 AAA1 Homo sapiens 71-74 17242399-0 2007 Sensor I threonine of the AAA+ ATPase transcriptional activator PspF is involved in coupling nucleotide triphosphate hydrolysis to the restructuring of sigma 54-RNA polymerase. Threonine 9-18 AAA1 Homo sapiens 26-37 17242399-0 2007 Sensor I threonine of the AAA+ ATPase transcriptional activator PspF is involved in coupling nucleotide triphosphate hydrolysis to the restructuring of sigma 54-RNA polymerase. nucleotide triphosphate 93-116 AAA1 Homo sapiens 26-37 18641692-4 2008 Western blot experiments showed that, whereas Bax expression was increased in pravastatin-incubated AAA explants, the expression of Bcl-2 was not modified. Pravastatin 78-89 AAA1 Homo sapiens 100-103 18641692-6 2008 In the human AAA explants, the increase in Bax expression, but not the increase in TIMP-1 expression elicited by pravastatin, was reversed by L-mevalonate, a downstream HMG-CoA reductase metabolite, suggesting that the expression of Bax and TIMP-1 followed HMG-CoA reductase-dependent and -independent pathways, respectively. l-mevalonate 142-154 AAA1 Homo sapiens 13-16 18641692-7 2008 In conclusion, pravastatin increases both TIMP-1 and Bax expression in human AAA explants without changes in either MMP-9 activity or the apoptotic status. Pravastatin 15-26 AAA1 Homo sapiens 77-80 18532870-3 2008 This paper describes a technique to manufacture realistic silicone AAA models for use with experimental studies. Silicones 58-66 AAA1 Homo sapiens 67-70 18532870-7 2008 Silicone rubber forms the basis of the resulting AAA model. Silicones 0-8 AAA1 Homo sapiens 49-52 17497968-3 2007 It is plausible that homocysteine may also play a role in the pathogenesis of abdominal aortic aneurysms (AAA) and that patients with this disease may benefit from folate supplementation. Homocysteine 21-33 AAA1 Homo sapiens 106-109 17242399-4 2007 We report activities for PspF(1-275) mutated in the AAA+ conserved sensor I threonine/asparagine motif (PspF(1-275)(T148A), PspF(1-275)(N149A), and PspF(1-275)(N149S)) within the second region of homology. Threonine 76-85 AAA1 Homo sapiens 52-55 17242399-4 2007 We report activities for PspF(1-275) mutated in the AAA+ conserved sensor I threonine/asparagine motif (PspF(1-275)(T148A), PspF(1-275)(N149A), and PspF(1-275)(N149S)) within the second region of homology. Asparagine 86-96 AAA1 Homo sapiens 52-55 16865521-6 2006 We gave the patient phenoxybenzamine, an alpha-blocker, preoperatively, then resected the adrenal mass and repaired the AAA. Phenoxybenzamine 20-36 AAA1 Homo sapiens 120-123 17244533-3 2007 We show that motif 2 of the ClpB M domain is positioned between the D1-large domains of neighboring subunits and could facilitate a concerted, ATP-driven conformational change in the AAA-1 ring. Adenosine Triphosphate 143-146 AAA1 Homo sapiens 183-188 17085593-3 2006 It has been proposed that during the ATP hydrolysis cycle, this tail domain swings against the AAA ring as a lever arm to generate the power stroke. Adenosine Triphosphate 37-40 AAA1 Homo sapiens 95-98 17182924-6 2006 We created a mouse AAA model by periaortic application of CaCl(2), which was accompanied by activation of JNK and MMPs, and suppression of lysyl oxidase (LOX), which is an essential biosynthetic enzyme for collagen and elastin fibers. Calcium Chloride 58-65 AAA1 Homo sapiens 19-22 17182924-8 2006 Treatment of mice with SP600125, a specific JNK inhibitor, completely abrogated the formation of CaCl(2)-induced AAA. pyrazolanthrone 23-31 AAA1 Homo sapiens 113-116 17182924-8 2006 Treatment of mice with SP600125, a specific JNK inhibitor, completely abrogated the formation of CaCl(2)-induced AAA. Calcium Chloride 97-104 AAA1 Homo sapiens 113-116 17182924-9 2006 Furthermore, SP600125 treatment after the establishment of AAA caused a reduction in the aortic diameters with normalized tissue architecture. pyrazolanthrone 13-21 AAA1 Homo sapiens 59-62 17182924-10 2006 SP600125 treatment also caused significant regression of angiotensin II-induced AAA in ApoE-null mice after its establishment, as demonstrated by serial ultrasonographic studies in live animals. pyrazolanthrone 0-8 AAA1 Homo sapiens 80-83 17244533-6 2007 Taken together, our results support a mechanism by which ClpB captures substrates on the upper surface of the AAA-1 ring before threading them through the ClpB hexamer in an ATP hydrolysis-driven step. Adenosine Triphosphate 174-177 AAA1 Homo sapiens 110-115 16973970-4 2006 Epidemiology studies suggest that smoking cessation and control of cholesterol and blood pressure should reduce the number of patients developing AAA. Cholesterol 67-78 AAA1 Homo sapiens 146-149 16722632-4 2006 Peptide analogues containing C(alpha alpha)-dialkylated glycine (Aaa1, 1) or C(alpha)-alkylated glycine (Aaa2, 2) amino acid residues showed antitumor activity against melanoma, larynx carcinoma, colon carcinomas, and colon metastasis cell lines in vitro. Glycine 56-63 AAA1 Homo sapiens 65-69 12761189-2 2003 Mutation of three amino acids, -Leu-Met-Tyr, at the carboxy-terminal end of the transmembrane segment of b5 to alanines resulted in localization of the mutated protein, b5LMY/AAA, in the cytosol as well as in the ER membrane. Leu-Met-Tyr 32-43 AAA1 Homo sapiens 169-178 15037237-4 2004 At least one AAA+ domain (AAA1) is capable of ATP binding and hydrolysis, and the available data suggest that one or more additional domains also may bind nucleotide. Adenosine Triphosphate 46-49 AAA1 Homo sapiens 26-30 12891121-13 2003 CONCLUSION: Stimulated expression of iNOS is associated with degeneration of AAA in human beings, and the activity of this enzyme under such conditions preferentially promotes formation and activity of peroxynitrite and further contributes to oxidative tissue and cellular injury in AAA. Peroxynitrous Acid 202-215 AAA1 Homo sapiens 77-80 12891121-13 2003 CONCLUSION: Stimulated expression of iNOS is associated with degeneration of AAA in human beings, and the activity of this enzyme under such conditions preferentially promotes formation and activity of peroxynitrite and further contributes to oxidative tissue and cellular injury in AAA. Peroxynitrous Acid 202-215 AAA1 Homo sapiens 283-286 15144675-3 2004 Seeding the cells to PTFE prostheses which implanted the abdominal aorta artery (AAA) and inferior vena cava (IVC). Polytetrafluoroethylene 21-25 AAA1 Homo sapiens 81-84 12761189-2 2003 Mutation of three amino acids, -Leu-Met-Tyr, at the carboxy-terminal end of the transmembrane segment of b5 to alanines resulted in localization of the mutated protein, b5LMY/AAA, in the cytosol as well as in the ER membrane. Alanine 111-119 AAA1 Homo sapiens 169-178 12761189-3 2003 When an N-glycosylation site was introduced at the carboxy-terminal end of b5LMY/AAA, a substantial amount of the glycosylated form of the mutant protein was recovered in the cytosol fraction. Nitrogen 8-9 AAA1 Homo sapiens 75-84 12553109-4 2002 The aim of this study was to investigate the effect of roxithromycin on the expansion rate of small AAA. Roxithromycin 55-68 AAA1 Homo sapiens 100-103 12553109-12 2002 Multiple linear regression analysis showed that roxithromycin treatment and initial AAA size were significantly related to AAA expansion when adjusted for smoking, diastolic blood pressure, and IgA level > or = 20. Roxithromycin 48-61 AAA1 Homo sapiens 123-126 12553109-14 2002 DISCUSSION: In comparison to placebo, roxithromycin 300 mg daily for four weeks reduced the expansion rate of AAA. Roxithromycin 38-51 AAA1 Homo sapiens 110-113 11718411-2 2001 METHOD: In an initial laboratory validation test, a silicone AAA model was imaged with a stereo-pair configuration of calibrated digital cameras using retro-reflective and ink dot surface targets. Silicones 52-60 AAA1 Homo sapiens 61-64 12208863-3 2002 Mice deficient in the expression of MMP-9 (MMP-9KO) or MMP-2 (MMP-2KO) and their corresponding wild-type background mice (WT) underwent AAA induction by abluminal application of calcium chloride (CaCl(2)). Calcium Chloride 178-194 AAA1 Homo sapiens 136-139 9579229-2 1998 It has been suggested that the ratio between branched-chain amino acids (BCAAs) and aromatic amino acids (AAAs) (BCAA/ AAA ratio) may determine in part the brain concentration of the AAAs, since the BCAAs compete with the AAAs for entry across the blood-brain barrier, leading to the accumulation of false neurotransmitters such as octopamine and phenylethanolamine, which are able to stimulate GH secretion (via alpha 2-adrenergic stimulation). Amino Acids, Aromatic 84-104 AAA1 Homo sapiens 106-109 11689524-5 2001 The prevalence of AAA defined by absolute diameter was higher than average in men born in The Netherlands or Scotland (more of whom had ever smoked or smoked currently) and lower in men of Mediterranean origin (more of whom drank alcohol currently). Alcohols 230-237 AAA1 Homo sapiens 18-21 10731425-1 2000 An arylalkylamine-type calmodulin antagonist, N-(3, 3-diphenylpropyl)-N"-[1-R-(3, 4-bis-butoxyphenyl)ethyl]-propylene-diamine (AAA) is presented and its complexes with calmodulin are characterized in solution and in the crystal. n-(3, 3-diphenylpropyl)-n"-[1-r-(3, 4-bis-butoxyphenyl)ethyl]-propylene-diamine 46-125 AAA1 Homo sapiens 127-130 10731425-4 2000 The binding of AAA causes domain closure of calmodulin similar to that obtained with trifluoperazine. Trifluoperazine 85-100 AAA1 Homo sapiens 15-18 10731425-5 2000 Solution and crystal data indicate that each of the two AAA molecules anchors in the hydrophobic pockets of calmodulin, overlapping with two trifluoperazine sites, i.e. at a hydrophobic pocket and an interdomain site. Trifluoperazine 141-156 AAA1 Homo sapiens 56-59 10651458-4 1999 Factors associated with AAA include smoking, age, coronary artery disease, high serum cholesterol level, family history, and hypertension. Cholesterol 86-97 AAA1 Homo sapiens 24-27 11596781-5 2001 ES were detected in 14.3% (2/14) of patients with AAA > or = 4 mm and in no patients with AAA < 4 mm or no AAA (p=0.14). Einsteinium 0-2 AAA1 Homo sapiens 50-53 11596781-6 2001 The findings suggest that ES may be associated with severe AAA but their prevalence is low in this setting. Einsteinium 26-28 AAA1 Homo sapiens 59-62 11345558-3 2001 Initial treatment of AAA should be made as early as possible and should associate high-dose oxygen, nebulisations of beta-2-agonists and corticosteroid infusion. Oxygen 92-98 AAA1 Homo sapiens 21-24 10392943-4 1999 We report a case of rectum and sigmoid colon necrosis with fatal outcome due to cholesterol embolization after implantation of a stent-graft for an infrarenal AAA. Cholesterol 80-91 AAA1 Homo sapiens 159-162 9756070-3 1998 MATERIALS AND METHODS: A life-sized AAA model was constructed of silicone elastomers with luminal access ports for introduction of contrast media and catheters. Silicones 65-73 AAA1 Homo sapiens 36-39 9579229-2 1998 It has been suggested that the ratio between branched-chain amino acids (BCAAs) and aromatic amino acids (AAAs) (BCAA/ AAA ratio) may determine in part the brain concentration of the AAAs, since the BCAAs compete with the AAAs for entry across the blood-brain barrier, leading to the accumulation of false neurotransmitters such as octopamine and phenylethanolamine, which are able to stimulate GH secretion (via alpha 2-adrenergic stimulation). Amino Acids, Branched-Chain 199-204 AAA1 Homo sapiens 106-109 9579229-2 1998 It has been suggested that the ratio between branched-chain amino acids (BCAAs) and aromatic amino acids (AAAs) (BCAA/ AAA ratio) may determine in part the brain concentration of the AAAs, since the BCAAs compete with the AAAs for entry across the blood-brain barrier, leading to the accumulation of false neurotransmitters such as octopamine and phenylethanolamine, which are able to stimulate GH secretion (via alpha 2-adrenergic stimulation). Octopamine 332-342 AAA1 Homo sapiens 106-109 9579229-2 1998 It has been suggested that the ratio between branched-chain amino acids (BCAAs) and aromatic amino acids (AAAs) (BCAA/ AAA ratio) may determine in part the brain concentration of the AAAs, since the BCAAs compete with the AAAs for entry across the blood-brain barrier, leading to the accumulation of false neurotransmitters such as octopamine and phenylethanolamine, which are able to stimulate GH secretion (via alpha 2-adrenergic stimulation). 2-amino-1-phenylethanol 347-365 AAA1 Homo sapiens 106-109 9012231-9 1996 Endoluminal repair of infrarenal AAA with use of Dacron covered nitinol stent-grafts is feasible, safe and clinically effective. Polyethylene Terephthalates 49-55 AAA1 Homo sapiens 33-36 8958991-4 1996 Recent studies using MMP-inhibiting tetracycline derivatives in the elastase-induced rodent model of AAA indicate that metalloproteinase suppression is a feasible and successful approach in the experimental setting. Tetracycline 36-48 AAA1 Homo sapiens 101-104 9012231-9 1996 Endoluminal repair of infrarenal AAA with use of Dacron covered nitinol stent-grafts is feasible, safe and clinically effective. nitinol 64-71 AAA1 Homo sapiens 33-36 7655973-8 1995 The prevalence of smoking, alcohol consumption, coronary heart disease, chronic obstructive pulmonary disease and arterial disease were significantly higher in patients with AAA (p < 0.01). Alcohols 27-34 AAA1 Homo sapiens 174-177 8060346-3 1994 The mutation at nucleotide pair 7444 converts stop codon AGA into lysine codon AAA (human mitochondrial genetic code). Lysine 66-72 AAA1 Homo sapiens 79-82 34075626-12 2021 After following 2 (range, 1-5) years, the AAA disappeared in one case with LAAA and two cases with RAAA. laaa 75-79 AAA1 Homo sapiens 42-45 1336709-3 1992 We now show that the osteosarcoma cell lines have lost one TP53 allele and contain a mutation in exon 8 codon 286 [GAA to AAA (Glu to Lys)] in the remaining allele. Glutamic Acid 127-130 AAA1 Homo sapiens 122-125 1336709-3 1992 We now show that the osteosarcoma cell lines have lost one TP53 allele and contain a mutation in exon 8 codon 286 [GAA to AAA (Glu to Lys)] in the remaining allele. Lysine 134-137 AAA1 Homo sapiens 122-125 2009986-5 1991 Tobacco and alcohol consumption, impaired lung function and a history of angina pectoris were related to the presence of an AAA. Alcohols 12-19 AAA1 Homo sapiens 124-127 33782614-2 2021 Here, we identify a triazolopyridine-based fragment that binds the AAA domain of human katanin, a microtubule-severing protein. CP-808844 20-36 AAA1 Homo sapiens 67-70 33782614-5 2021 Importantly, ASPIR-1 also selectively inhibits engineered cysteine mutants of human VPS4B and FIGL1-AAA proteins, involved in organelle dynamics and genome stability, respectively. Cysteine 58-66 AAA1 Homo sapiens 100-103 8170049-1 1994 PURPOSE: The purpose of this study was to test the hypothesis that abdominal aortic aneurysms (AAA) whose morphology makes them unsuited for repair with an endoluminal tube graft can be treated by a combination of a transluminally placed aortofemoral graft and a femorofemoral crossover graft. aortofemoral 238-250 AAA1 Homo sapiens 95-98 35621206-1 2022 Background Elevated plasma levels of alpha-aminoadipic acid (2-AAA) have been associated with the development of type 2 diabetes and atherosclerosis. 2-Aminoadipic Acid 37-59 AAA1 Homo sapiens 63-66 34139912-15 2021 CONCLUSION: At the early stage of AAA, the current study indicated the importance of glycosaminoglycan degradation and anaerobic metabolism. Glycosaminoglycans 85-102 AAA1 Homo sapiens 34-37 35621206-8 2022 We further characterized the genetically predicted relationship through measurement of plasma 2-AAA and high-density lipoprotein cholesterol in 2 separate samples of individuals with and without cardiometabolic disease (N=98), and confirmed a significant negative correlation between 2-AAA and high-density lipoprotein (rs=-0.53, P<0.0001). Cholesterol 129-140 AAA1 Homo sapiens 286-289 35621206-10 2022 Elevated plasma 2-AAA associates with reduced levels of high-density lipoprotein cholesterol. Cholesterol 81-92 AAA1 Homo sapiens 18-21 35552390-5 2022 These findings support the model that p97 utilizes a "hand-over-hand" mechanism in which two residues of the substrate are translocated for hydrolysis of two ATPs, one in each of the two p97 AAA ATPase rings. Adenosine Triphosphate 158-162 AAA1 Homo sapiens 191-194