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Journal articles on the topic 'Aggregation induced'

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Published: 7 July 2024

Last updated: 31 July 2025

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1

Kelton, JG, JC Moore, and WG Murphy. "Studies investigating platelet aggregation and release initiated by sera from patients with thrombotic thrombocytopenic purpura." Blood 69, no. 3 (1987): 924–28. http://dx.doi.org/10.1182/blood.v69.3.924.924.

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Abstract Many patients with thrombotic thrombocytopenic purpura (TTP) have a platelet aggregating factor in their serum that may be pathologically linked with the disease process. To help characterize the type of platelet aggregation and platelet release induced by the sera from seven TTP patients, we measured the ability of a variety of inhibitors of platelet function as well as the ability of monoclonal antibodies (MoAbs) against platelet glycoproteins to inhibit TTP sera-induced platelet aggregation and release. These results were compared with the ability of the same inhibitors to block pl

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2

Kelton, JG, JC Moore, and WG Murphy. "Studies investigating platelet aggregation and release initiated by sera from patients with thrombotic thrombocytopenic purpura." Blood 69, no. 3 (1987): 924–28. http://dx.doi.org/10.1182/blood.v69.3.924.bloodjournal693924.

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Many patients with thrombotic thrombocytopenic purpura (TTP) have a platelet aggregating factor in their serum that may be pathologically linked with the disease process. To help characterize the type of platelet aggregation and platelet release induced by the sera from seven TTP patients, we measured the ability of a variety of inhibitors of platelet function as well as the ability of monoclonal antibodies (MoAbs) against platelet glycoproteins to inhibit TTP sera-induced platelet aggregation and release. These results were compared with the ability of the same inhibitors to block platelet ag

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3

YAGER, RONALD R. "CHOQUET AGGREGATION USING ORDER INDUCING VARIABLES." International Journal of Uncertainty, Fuzziness and Knowledge-Based Systems 12, no. 01 (2004): 69–88. http://dx.doi.org/10.1142/s0218488504002667.

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We discuss the OWA and Choquet integral aggregation operators and point out the central role the ordering operation plays in these operators. We extend the capabilities of the Choquet integral aggregation by allowing the ordering to be induced by some values other then those being aggregated. This allows us to consider an induced Choquet Choquet integral aggregation operator. We look at the properties of this operator. We then look at its applications. Among the applications considered are aggregations guided by linguistic and other ordinal structures. We look at the use of induced aggregation

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4

Teng, Che-Ming, Ya-Fei Kang, Ya-Ling Chang, Feng-Nien Ko, Shu-Chen Yang, and Feng-Lin Hsu. "ADP-mimicking Platelet Aggregation Caused by Rugosin E, an Ellagitannin Isolated from Rosa rugosa Thunb." Thrombosis and Haemostasis 77, no. 03 (1997): 555–61. http://dx.doi.org/10.1055/s-0038-1656005.

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SummaryAmong the nine ellagitannins, rugosin E was the most potent platelet aggregating agent with an EC50 of 1.5 ± 0.1 µM in rabbit platelets and 3.2 ±0.1 µM in human platelets. The aggregations caused by rugosin E and ADP were inhibited by EGTA, PGE1, mepacrine, sodium nitroprusside and neomycin, but not by indomethacin, verapamil, TMB-8, BN52021 and GR32191B. Rugosin E-induced thromboxane formation was suppressed by indomethacin, EGTA, PGE,, verapamil, mepacrine, TMB-8 and neomycin. ADP-scavenging agents, such as CP/CPK and apyrase inhibited concentration-dependently ADP (20 εM)-, but not r

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5

Huang, T. F., C. Z. Liu, and S. H. Yang. "Aggretin, a novel platelet-aggregation inducer from snake (Calloselasma rhodostoma) venom, activates phospholipase C by acting as a glycoprotein Ia/IIa agonist." Biochemical Journal 309, no. 3 (1995): 1021–27. http://dx.doi.org/10.1042/bj3091021.

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A potent platelet aggregation inducer, aggretin, was purified from Malayan-pit-viper (Calloselasma rhodostoma) venom by ionic-exchange chromatography, gel-filtration chromatography and HPLC. It is a heterodimeric protein (29 kDa) devoid of esterase, phospholipase A and thrombin-like activity. Aggretin (> 5 nM) elicited platelet aggregation with a lag period in both human platelet-rich plasma and washed platelet suspension. EDTA (5 mM), prostaglandin E1 (1 microM) and 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (‘TMB-8’; 100 microM) abolished its aggregating activity, indicating

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6

Kariyazono, Hiroko, Kazuo Nakamura, Terutoshi Shinkawa, et al. "Inhibitory effects of antibiotics on platelet aggregation in vitro." Human & Experimental Toxicology 16, no. 11 (1997): 662–66. http://dx.doi.org/10.1177/096032719701601106.

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1 We evaluated in vitro inhibitory effects of six types of antibiotic, aztreonam (AZT), cefamandole (CMD), cefmetazole (CMZ), cefotiam (CTM), flomoxef (FMOX) and latamoxef (LMOX), on platelet aggregation, using healthy volunteers' blood. Four types-FMOX, LMOX, CTM and CMD-inhibited, in concentration of 2500 ?g/ml, the secondary aggregation induced by 3.0 ?M adenosine diphosphate (ADP), and also inhibited the aggregation induced by 0.5 ?g/ml collagen. AZT in the same concentration, did not inhibit the aggregation induced by collagen, and it inhibited only ADP induced aggregation. CMZ, in the sa

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7

Sugiyama, T., M. Okuma, F. Ushikubi, S. Sensaki, K. Kanaji, and H. Uchino. "A novel platelet aggregating factor found in a patient with defective collagen-induced platelet aggregation and autoimmune thrombocytopenia." Blood 69, no. 6 (1987): 1712–20. http://dx.doi.org/10.1182/blood.v69.6.1712.1712.

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Abstract We found a novel platelet aggregating factor in a patient with steroid- responsive immune thrombocytopenic purpura that is associated with defective collagen-induced platelet functions. The aggregating factor and platelet functions were analyzed. The patient, a 58-year-old female, had purpura and prolonged bleeding time despite adequate platelet counts (greater than 140,000/microL) after steroid therapy. The patient's platelets responded normally to all agonists except collagen. Platelet adhesion to collagen fibrils was decreased. The patient's plasma induced irreversible aggregation

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8

Sugiyama, T., M. Okuma, F. Ushikubi, S. Sensaki, K. Kanaji, and H. Uchino. "A novel platelet aggregating factor found in a patient with defective collagen-induced platelet aggregation and autoimmune thrombocytopenia." Blood 69, no. 6 (1987): 1712–20. http://dx.doi.org/10.1182/blood.v69.6.1712.bloodjournal6961712.

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We found a novel platelet aggregating factor in a patient with steroid- responsive immune thrombocytopenic purpura that is associated with defective collagen-induced platelet functions. The aggregating factor and platelet functions were analyzed. The patient, a 58-year-old female, had purpura and prolonged bleeding time despite adequate platelet counts (greater than 140,000/microL) after steroid therapy. The patient's platelets responded normally to all agonists except collagen. Platelet adhesion to collagen fibrils was decreased. The patient's plasma induced irreversible aggregation and ATP r

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9

Nakamura, K., H. Kariyazono, T. Shinkawal, et al. "Inhibitory effects of H2-receptor antagonists on platelet function in vitro." Human & Experimental Toxicology 18, no. 8 (1999): 487–92. http://dx.doi.org/10.1191/096032799678847069.

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1 To evaluate in vitro inhibitory effects of four types of histamine H2-receptor antagonist (H2-receptor antagonists), famotidine, roxatidine, cimetidine and ranitidine, on platelet function, we examined aggregating potency and P-selectin levels with agonist-induced aggregation. Ranitidine and cimetidine inhibited, in concentration of 0.35 mM, the secondary aggregation induced by 5 pM adenosine diphosphate (ADP), the aggregation induced by 1,g/mL collagen and 3 gM arachidonic acid. All of H2-receptor antagonists inhibited, in concentration of 1.4 mm, the aggregation induced by ADP, collagen an

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10

Higashihara, M., H. Maeda, Y. Shibata, S. Kume, and T. Ohashi. "A monoclonal anti-human platelet antibody: a new platelet aggregating substance." Blood 65, no. 2 (1985): 382–91. http://dx.doi.org/10.1182/blood.v65.2.382.382.

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Abstract A monoclonal anti-human platelet antibody, TP82, is described, which caused irreversible aggregation of platelets in association with the release of adenosine triphosphate or [14C] serotonin, and which inhibited ristocetin-induced agglutination. Immunofluorescence assay showed that the antibody binds to platelets, megakaryocytes, and common acute lymphoblastic leukemia cells. The antibody (IgG1) immunoprecipitated a polypeptide of 23,000 daltons with an isoelectric point of about 7.0. The aggregation induced by the purified antibody and/or F(ab')2 fragments occurred in platelet-rich p

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11

Higashihara, M., H. Maeda, Y. Shibata, S. Kume, and T. Ohashi. "A monoclonal anti-human platelet antibody: a new platelet aggregating substance." Blood 65, no. 2 (1985): 382–91. http://dx.doi.org/10.1182/blood.v65.2.382.bloodjournal652382.

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A monoclonal anti-human platelet antibody, TP82, is described, which caused irreversible aggregation of platelets in association with the release of adenosine triphosphate or [14C] serotonin, and which inhibited ristocetin-induced agglutination. Immunofluorescence assay showed that the antibody binds to platelets, megakaryocytes, and common acute lymphoblastic leukemia cells. The antibody (IgG1) immunoprecipitated a polypeptide of 23,000 daltons with an isoelectric point of about 7.0. The aggregation induced by the purified antibody and/or F(ab')2 fragments occurred in platelet-rich plasma and

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12

Tang, B., Z. Zhao, Z. Wang, et al. "Aggregation-Induced Emission." Synfacts 2009, no. 12 (2009): 1345. http://dx.doi.org/10.1055/s-0029-1218183.

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13

Yager, Ronald R. "Induced aggregation operators." Fuzzy Sets and Systems 137, no. 1 (2003): 59–69. http://dx.doi.org/10.1016/s0165-0114(02)00432-3.

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14

Hong, Yuning, Jacky W. Y. Lam, and Ben Zhong Tang. "Aggregation-induced emission." Chemical Society Reviews 40, no. 11 (2011): 5361. http://dx.doi.org/10.1039/c1cs15113d.

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15

Packham, M. A., A. A. Livne, D. H. Ruben, and M. L. Rand. "Activation of phospholipase C and protein kinase C has little involvement in ADP-induced primary aggregation of human platelets: effects of diacylglycerols, the diacylglycerols, the diacylglycerol kinase inhibitor R59022, staurosporine and okadaic acid." Biochemical Journal 290, no. 3 (1993): 849–56. http://dx.doi.org/10.1042/bj2900849.

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The primary phase of ADP-induced aggregation of human platelets does not involve appreciable formation of thromboxane A2 or release of granule contents; lack of formation of inositol trisphosphate has also been noted. Because these responses of platelets to ADP differ so markedly from their responses to other aggregating agents, the roles in ADP-induced aggregation of diacylglycerol, protein kinase C, increases in cytosolic [Ca2+], phosphorylation of pleckstrin (47 kDa) and phosphatases 1 and 2a were investigated. Washed human platelets, prelabelled with [14C]5-hydroxytryptamine and suspended

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16

Natella, F., M. Nardini, F. Belelli, et al. "Effect of coffee drinking on platelets: inhibition of aggregation and phenols incorporation." British Journal of Nutrition 100, no. 6 (2008): 1276–82. http://dx.doi.org/10.1017/s0007114508981459.

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Epidemiological studies indicate a J-shaped relationship linking coffee consumption and cardiovascular risk, suggesting that moderate coffee consumption can be beneficial. Platelet aggregation is of critical importance in thrombotic events, and platelets play a major role in the aetiology of several CVD. The aim of this study was to evaluate the effect of coffee drinking on platelet aggregationex vivo, using caffeine as control. A crossover study was performed on ten healthy subjects. In two different sessions, subjects drank 200 ml coffee, containing 180 mg caffeine, or a capsule of caffeine

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17

Teng, Che-Ming, and Feng-Nien Ko. "Comparison of the Platelet Aggregation Induced by Three Thrombin-Like Enzymes of Snake Venoms and Thrombin." Thrombosis and Haemostasis 59, no. 02 (1988): 304–9. http://dx.doi.org/10.1055/s-0038-1642776.

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SummaryPlatelet aggregation induced by three thrombin-like enzymes of snake venoms was compared with that by thrombin. Acutin was isolated from Agkistrodon acutus venom and thrombocytin and batroxobin were from Bothrops atrox venom. The fibrinogenclotting activities were 700,170 and 7 U/mg for batroxobin, acutin and thrombocytin, respectively. They induced aggregation and ATP release of washed rabbit platelets. The aggregating activity of thrombin was 102, 104 and 105 times more potent than those of thrombocytin, acutin and batroxobin, respectively. Plateletactivating potency of the thrombin-l

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18

Lian, EC, and FA Siddiqui. "Investigation of the role of von Willebrand factor in thrombotic thrombocytopenic purpura." Blood 66, no. 5 (1985): 1219–21. http://dx.doi.org/10.1182/blood.v66.5.1219.1219.

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Abstract Von Willebrand factor (vWF) has been implicated to function as a cofactor in platelet aggregation induced by thrombotic thrombocytopenic purpura (TTP) plasma. To investigate further this role of vWF, we have used rabbit monospecific anti-FVIII/vWF antibodies and a monoclonal antibody to platelet glycoprotein Ib (GP Ib) that blocks the ristocetin- induced platelet aggregation. The monoclonal anti-platelet GP Ib antibody inhibited the platelet aggregation induced by ristocetin in the presence of normal plasma, but not that by any of the five TTP plasma samples. The TTP plasma samples fr

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19

Lian, EC, and FA Siddiqui. "Investigation of the role of von Willebrand factor in thrombotic thrombocytopenic purpura." Blood 66, no. 5 (1985): 1219–21. http://dx.doi.org/10.1182/blood.v66.5.1219.bloodjournal6651219.

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Von Willebrand factor (vWF) has been implicated to function as a cofactor in platelet aggregation induced by thrombotic thrombocytopenic purpura (TTP) plasma. To investigate further this role of vWF, we have used rabbit monospecific anti-FVIII/vWF antibodies and a monoclonal antibody to platelet glycoprotein Ib (GP Ib) that blocks the ristocetin- induced platelet aggregation. The monoclonal anti-platelet GP Ib antibody inhibited the platelet aggregation induced by ristocetin in the presence of normal plasma, but not that by any of the five TTP plasma samples. The TTP plasma samples from five p

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20

Vigil, R. Dennis, Isaac Vermeersch, and Rodney O. Fox. "Destructive aggregation: Aggregation with collision-induced breakage." Journal of Colloid and Interface Science 302, no. 1 (2006): 149–58. http://dx.doi.org/10.1016/j.jcis.2006.05.066.

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21

Barzaghi, Giovanna, Chiara Cerletti, and Giovanni de Gaetano. "Phospholipase C from Clostridium Perfringens Induces Human Platelet Aggregation in Plasma." Thrombosis and Haemostasis 59, no. 02 (1988): 236–39. http://dx.doi.org/10.1055/s-0038-1642761.

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SummaryWe studied the aggregating effect of different concentrations of phospholipase C (PLC) (extracted from Clostridium perfringens) on human platelet-rich plasma (PRP). PRP was preincubated with PLC for 3 min at 37° C and the platelet aggregation was followed for 10 min. The threshold aggregating concentration (TAG) of PLC was 3-4 U/ml.We also studied the potentiation of PLC with other stimuli on platelet aggregation. Potentiating stimuli, such as arachidonic acid (AA), ADP. Platelet Activating Factor (PAF) and U-46619 (a stable analogue of cyclic endoperoxides) were all used at subthreshol

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22

Chiang, T. M., A. Jin, and A. H. Kang. "Platelet-collagen interaction. Inhibition by a monoclonal antibody raised against collagen receptor." Journal of Immunology 139, no. 3 (1987): 887–92. http://dx.doi.org/10.4049/jimmunol.139.3.887.

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Abstract Monoclonal antibodies to the purified platelet type I collagen receptor were produced to study platelet receptor function. The antibody specifically reacted with the platelet receptor in immunoblot experiments. The IgG purified from the monoclonal antibodies and isolated Fab' fragments inhibited the binding of radiolabeled alpha 1(I) chain to washed platelets competitively. Soluble and fibrillar type I collagen-induced platelet aggregations were inhibited by purified IgG suggesting that soluble and fibrillar collagens shared a common receptor. The adhesion of platelets to an artificia

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23

Barr, Stephen C., John W. Ludders, Andrea L. Looney, Robin D. Gleed, and Hollis N. Erb. "Platelet aggregation in dogs after sedation with acepromazine and atropine and during subsequent general anesthesia and surgery." American Journal of Veterinary Research 53, no. 11 (1992): 2067–70. http://dx.doi.org/10.2460/ajvr.1992.53.11.2067.

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Summary Platelet aggregation and adenosine triphosphate (atp) release were measured by use of the impedance method in blood samples obtained from 25 adult female Beagles before and after sedation with acepromazine (0.13 mg/kg of body weight) and atropine (0.05 mg/kg), and during general anesthesia. General anesthesia was induced by iv administration of thiamylal (average dosage, 2.1 mg/kg; range, 1.2 to 4.2 mg/kg) and was maintained with halothane in oxygen. Samples of jugular venous blood were obtained from each dog, using citrate as anticoagulant. Platelet count was done on each sample. Plat

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24

Surapinit, Serm, and Nuttakorn Baisaeng. "Macrostachyols A-D, oligostilbenes from Gnetum macrostachyum inhibited in vitro human platelet aggregation." Journal of Herbmed Pharmacology 10, no. 3 (2021): 339–43. http://dx.doi.org/10.34172/jhp.2021.39.

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Introduction: Gnetum macrostachyum is a known Thai medicinal plant as a source of bioactive oligostilbenes, which possess platelet inhibitory activities. The study aimed to evaluate the in vitro human platelet aggregation inhibitory activities of macrostachyols A-D (compounds 1-4) isolated from the roots of G. macrostachyum. Methods: The in vitro human platelet aggregation assay was assayed with a 96-well microtiter plate format. The well-known aggregating agents were used to investigate the possible mechanism of inhibition, including adenosine diphosphate (ADP), arachidonic acid (AA), thrombo

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25

CALZADA, Catherine, Evelyne VERICEL, and Michel LAGARDE. "Low concentrations of lipid hydroperoxides prime human platelet aggregation specifically via cyclo-oxygenase activation." Biochemical Journal 325, no. 2 (1997): 495–500. http://dx.doi.org/10.1042/bj3250495.

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There is mounting evidence that lipid peroxides contribute to pathophysiological processes and can modulate cellular functions. The aim of the present study was to investigate the effects of lipid hydroperoxides on platelet aggregation and arachidonic acid (AA) metabolism. Human platelets, isolated from plasma, were incubated with subthreshold (i.e. non-aggregating) concentrations of AA in the absence or presence of hydroperoxyeicosatetraenoic acids (HPETEs). Although HPETEs alone had no effect on platelet function, HPETEs induced the aggregation of platelets co-incubated with non-aggregating

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26

Whitin, J. C., and H. J. Cohen. "Dissociation between aggregation and superoxide production in human granulocytes." Journal of Immunology 134, no. 2 (1985): 1206–11. http://dx.doi.org/10.4049/jimmunol.134.2.1206.

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Abstract Aggregation and the activation of the granulocyte (PMN) superoxide (O2-) generating system occur when certain stimuli are added to resting cells. It had previously been postulated that PMN aggregation is essential for maximal O2- production. This study was undertaken to test the hypothesis that PMN aggregation is required for full expression of PMN O2- production. We examined aggregation and O2- production induced by four stimuli; concanavalin A (Con A), phorbol myristate acetate (PMA), N-formylmethionyl-leucyl-phenylalanine (FMLP), and ionophore A23187. Cytochalasin B enhanced aggreg

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27

Zhang, Yun-Xiang, Ting-Ting Yang, Liu Xia, Wei-Fen Zhang, Jia-Fu Wang, and Ya-Ping Wu. "Inhibitory Effect of Propolis on Platelet Aggregation In Vitro." Journal of Healthcare Engineering 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/3050895.

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Platelet hyperactivity plays an important role in arterial thrombosis and atherosclerosis. The present study was aimed to investigate the effects of different extracts of propolis and components of flavonoids on platelet aggregation. Platelet-rich plasma was prepared and incubated in vitro with different concentrations of the tested extracts and components of flavonoids. Platelets aggregation was induced by different agonists including adenosine diphosphate (ADP, 10 μM), thrombin receptor activator peptide (TRAP, 50 μM), and collagen (5 μg/mL). At 25 mg/L to 300 mg/mL, the water extract propol

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28

Yan, Yan, and Julián F. Hillyer. "The immune and circulatory systems are functionally integrated across insect evolution." Science Advances 6, no. 48 (2020): eabb3164. http://dx.doi.org/10.1126/sciadv.abb3164.

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The immune and circulatory systems of mammals are functionally integrated, as exemplified by the immune function of the spleen and lymph nodes. Similar functional integration exists in the malaria mosquito, Anopheles gambiae, as exemplified by the infection-induced aggregation of hemocytes around the heart valves. Whether this is specific to mosquitoes or a general characteristic of insects remained unknown. We analyzed 68 species from 51 families representing 16 orders and found that infection induces the aggregation of hemocytes and pathogens on the heart of insects from all major branches o

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29

Nie, Han, Kun Hu, Yuanjing Cai, et al. "Tetraphenylfuran: aggregation-induced emission or aggregation-caused quenching?" Materials Chemistry Frontiers 1, no. 6 (2017): 1125–29. http://dx.doi.org/10.1039/c6qm00343e.

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Tetraphenylfuran, structurally similar to AIE-active siloles, exhibits the traditional aggregation-caused quenching, which is co-caused by the restriction of intramolecular rotation and the conjugation effect.

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Lin, Po-An, Hsiang-Han Huang, Mei-Hua Hu, et al. "Prostate Tissue-Induced Platelet Activation and Platelet–Neutrophil Aggregation Following Transurethral Resection of the Prostate Surgery: An In Vitro Study." Biomedicines 13, no. 4 (2025): 1006. https://doi.org/10.3390/biomedicines13041006.

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Background: This study aimed to investigate the effects of prostate tissue on platelet activation markers, primarily assessed through P-selectin expression, and to assess the formation of platelet–leukocyte aggregations in response to prostate tissue exposure. Furthermore, we compared platelet activation induced by prostate tissue homogenates with that induced by thrombin stimulation. These processes may play a role in the development of disseminated intravascular coagulation (DIC) following transurethral resection of the prostate (TURP). Methods: We collected prostate tissue samples from 12 p

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Hornberger, Zachary, Bruce Cox, and Raymond R. Hill. "Analysis of the effects of spatiotemporal demand data aggregation methods on distance and volume errors." Journal of Defense Analytics and Logistics 5, no. 1 (2021): 29–45. http://dx.doi.org/10.1108/jdal-03-2020-0003.

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Purpose Large/stochastic spatiotemporal demand data sets can prove intractable for location optimization problems, motivating the need for aggregation. However, demand aggregation induces errors. Significant theoretical research has been performed related to the modifiable areal unit problem and the zone definition problem. Minimal research has been accomplished related to the specific issues inherent to spatiotemporal demand data, such as search and rescue (SAR) data. This study provides a quantitative comparison of various aggregation methodologies and their relation to distance and volume b

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Zhang, Zechen, Jared R. Arkfeld, and William A. Ducker. "Proximity-induced surfactant aggregation." Colloid and Interface Science Communications 50 (September 2022): 100657. http://dx.doi.org/10.1016/j.colcom.2022.100657.

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ZELLER, J. A., RUTH E. DAYHOFF, K. EURENIUS, W. RUSSELL, and R. S. LEDLEY. "Aldehyde-induced platelet aggregation." Clinical & Laboratory Haematology 6, no. 2 (2008): 145–55. http://dx.doi.org/10.1111/j.1365-2257.1984.tb00537.x.

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34

O'Brien, J. R. "Shear-induced platelet aggregation." Lancet 335, no. 8691 (1990): 711–13. http://dx.doi.org/10.1016/0140-6736(90)90815-m.

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35

Liu, Hao, Jingjing Guo, Zujin Zhao, and Ben Zhong Tang. "Aggregation‐Induced Delayed Fluorescence." ChemPhotoChem 3, no. 10 (2019): 993–99. http://dx.doi.org/10.1002/cptc.201900118.

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36

Wallén, N. Håkan, Claes Held, Nina Rehnqvist, and Paul Hjemdahl. "Impact of Treatment with Acetylsalicylic Acid on the Proaggregatory Effects of Adrenaline in vitro in Patients with Stable Angina Pectoris: Influence of the Anticoagulant." Clinical Science 85, no. 5 (1993): 577–83. http://dx.doi.org/10.1042/cs0850577.

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1. The impact of oral acetylsalicylic acid treatment on the enhancing effect of adrenaline on platelet aggregation in vitro was investigated in patients with stable angina pectoris. In addition, the influence of different anticoagulants (i.e. hirudin and citrate) on platelet aggregation in vitro was compared. 2. Eighty-four patients with stable angina pectoris were studied. Sixteen patients were on acetylsalicylic acid treatment (150-250 mg daily), whereas 68 patients were free from acetylsalicylic acid. Platelet-rich-plasma was prepared from citrate- or hirudin-antkoagulated blood. The EC50 (

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37

Watson, Ben R., Nathan A. White, Kirk A. Taylor, et al. "Zinc is a transmembrane agonist that induces platelet activation in a tyrosine phosphorylation-dependent manner." Metallomics 8, no. 1 (2016): 91–100. http://dx.doi.org/10.1039/c5mt00064e.

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38

Bhat, Waseem Feeroze, Azaj Ahmed, Shabeena Abbass, Mohammad Afsar, Bilqees Bano, and Akbar Masood. "Deciphering the Nature of Caffeic Acid to Inhibit the HSA Aggregation Induced by Glyoxal." Protein & Peptide Letters 27, no. 8 (2020): 725–35. http://dx.doi.org/10.2174/0929866527666200129105141.

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Background: Under certain circumstances, the path for protein folding deviates and attains an alternative path forming misfolded states, which are the key precursors for protein aggregation. Protein aggregation is associated with variety of diseases and leads to the cytotoxicity. These protein aggregate related diseases have been untreated so far. However, extensive attempts have been applied to develop anti-aggregating agents as possible approaches to overcome protein aggregation. Different types of substances have been reported to halt or decrease the formation of ordered protein aggregates

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39

McCulloch, R. K., J. Summers, R. Vandongen, and I. L. Rouse. "Role of Thromboxane A2 as a Mediator of Platelet-Activating-Factor-Induced Aggregation of Human Platelets." Clinical Science 77, no. 1 (1989): 99–103. http://dx.doi.org/10.1042/cs0770099.

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1. At present it is unclear whether platelet-activating-factor (PAF)-induced aggregation is mediated by thromboxane. To obtain further information about this event we have compared the affects of aspirin on platelet aggregation and secretion induced by PAF and collagen. 2. Collagen and PAF induced aggregation and secretion in human platelets in a dose-related manner. 3. Aspirin inhibited the magnitude of both platelet aggregation and secretion induced by PAF and collagen, but the degree of inhibition was much greater for collagen. 4. Aspirin strongly inhibited the aggregation rate of collagen-

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Trubacheva, O. A., I. V. Kologrivova, T. E. Suslova, A. V. Swarovskaya, and A. A. Garganeeva. "Platelet aggregation under the conditions of vortex flow in vitro in patients with chronic heart failure." Bulletin of Siberian Medicine 21, no. 2 (2022): 122–28. http://dx.doi.org/10.20538/1682-0363-2022-2-122-128.

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Aim. To compare the effect of increased concentrations of aggregation inducers (five-fold addition) under standard conditions and under the conditions of vortex flow in vitro on platelet aggregation in patients with chronic heart failure (CHF).Materials and methods. The study included 28 patients. The activity of platelet aggregation in platelet-rich plasma (PRP) was evaluated according to light transmission curves (%) and the average size of aggregates (relative units (rel. units)). The aggregation inducer was added once at 10 seconds of the study (standard procedure) and five times at 10 sec

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Dembélé-Duchesne, M. J., A. Laghchim Lahlou, H. Thaler-Dao, and A. Crastes de Paulet. "Inhibition of Platelet Aggregation by Human Placenta." Thrombosis and Haemostasis 54, no. 02 (1985): 431–37. http://dx.doi.org/10.1055/s-0038-1657866.

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SummaryHuman placental cytosol inhibits platelet aggregation induced by high doses of collagen. The aim of this study was to investigate whether this anti-aggregating activity was caused only by the presence of various activities already described in the placenta (an ADP-consuming enzyme, a fatty acid cyclooxygenase inhibitor, and a thromboxane synthetase inhibitor) or whether another factor was present.Heating the cytosol at 50° C for 6 min destroyed the inhibitor of collagen-induced aggregation. ADPase and the AA pathway inhibitors were not modified by this treatment. We therefore show the p

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Rosenfeldt, Mathias, Michael Valentino, Salvatore Labruzzo, et al. "The organomercurial 4-aminophenylmercuric acetate, independent of matrix metalloproteinases, induces dose-dependent activation/ inhibition of platelet aggregation." Thrombosis and Haemostasis 93, no. 02 (2005): 326–30. http://dx.doi.org/10.1160/th04-08-0541.

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SummaryMatrix metalloproteinases (MMPs) play an important role in many biological and pathological processes including tissue remodeling, wound healing, inflammation, atherosclerosis, and cancer. Numerous publications have supported the concept that activated MMP-2 enhances agonist-induced platelet aggregation and activated MMP-9 inhibits platelet aggregation. In this study, we demonstrated that the organomercurial compound, 4-aminophenyl mercuric acetate (APMA), which is routinely employed to activate latent MMPs at a concentration of 1000 μ M, induces platelet aggregation at low concentratio

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Del Zar, María de las M., Marta Martinuzzo, Daniel P. Cardinali, Luis O. Carreras, and María I. Vacas. "Diurnal variation in melatonin effect on adenosine triphosphate and serotonin release by human platelets." Acta Endocrinologica 123, no. 4 (1990): 453–58. http://dx.doi.org/10.1530/acta.0.1230453.

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Abstract. The effect of the pineal hormone melatonin on adenosine diphosphate-induced human platelet aggregation and adenosine triphosphate release was assessed in platelet-rich plasma obtained from normal volunteers at 08.30 and 20.30 h. In 10−7-10−5 mol/l concentrations melatonin inhibited ADP-induced platelet aggregation only in the evening (p<0.05). ADP-induced ATP release, an index of platelet secretory processes, showed a generally greater, dose-dependent inhibition after adding melatonin (10−9-10−5 mol/l) at 20.30 h as compared with 08.30 h. The inhibitory activity of melatonin (10−9

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Ott, C., E. Lardi, T. Schulzki, and W. H. Reinhart. "The influence of erythrocyte aggregation on induced platelet aggregation." Clinical Hemorheology and Microcirculation 45, no. 2-4 (2010): 375–82. http://dx.doi.org/10.3233/ch-2010-1319.

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Kinlough-Rathbone, R. L., D. W. Perry, M. L. Rand, and M. A. Packham. "Pretreatment of Human Platelets with Plasmin Inhibits Responses toThrombin, but Potentiates Responses to Low Concentrations of Aggregating Agents, Including the Thrombin Receptor Activating Peptide, SFLLRN." Thrombosis and Haemostasis 77, no. 04 (1997): 741–47. http://dx.doi.org/10.1055/s-0038-1656044.

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SummaryEffects of plasmin on platelets, that influence subsequent responses to aggregating agents, are relevant to attempts to prevent rethrombosis following administration of fibrinolytic agents. We describe plasmin-induced inhibition of platelet responses to thrombin, but potentiation of responses to other aggregating agents. Washed human platelets were labeled with 14C-serotonin, treated for 30 min at 37° C with 0, 0.1 or 0.2 CU/ml of plasmin, followed by aprotinin, washed and resuspended in a Tyrode-albumin solution with apyrase. Incubation with 0.2 CU/ml of plasmin almost completely inhib

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XIA, MEIMEI, ZESHUI XU, and NA CHEN. "INDUCED AGGREGATION UNDER CONFIDENCE LEVELS." International Journal of Uncertainty, Fuzziness and Knowledge-Based Systems 19, no. 02 (2011): 201–27. http://dx.doi.org/10.1142/s0218488511006976.

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This paper proposes a series of aggregation operators considering the confidence levels of the aggregated arguments. Due to the complex connections among the arguments, we further give two nonlinear aggregation operators and discuss their properties. Then we extend these aggregation operators to hesitant fuzzy environments in which there are some difficulties in determining the membership of an element to a set. Several numerical examples are used to compare the proposed aggregation operators.

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Khan, Javed Masood, Ajamaluddin Malik, Fohad Mabood Husain, Mohammed J. Hakeem та Abdullah S. Alhomida. "Sunset Yellow Dye Induces Amorphous Aggregation in β-Lactoglobulin at Acidic pH: A Multi-Techniques Approach". Polymers 14, № 3 (2022): 395. http://dx.doi.org/10.3390/polym14030395.

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Protein aggregation is of two types: (i) amorphous and (ii) amyloid fibril. Several extrinsic factors (temperature, pH, and small ligands) stimulate protein aggregation in vitro. In this study, we have examined the role of sunset yellow (SY) on the β-lactoglobulin (BLG) aggregation at pH 2.0. We have used spectroscopic (turbidity, Rayleigh light scattering (RLS), far-UV CD) and microscopic (transmission electron microscopy [TEM]) techniques to describe the effects of SY on BLG aggregation. Our results showed that BLG aggregation is dependent on SY concentrations. Very low concentrations (0.0–0

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Bassani, Ilaria, Corinne Rancurel, Sophie Pagnotta, et al. "Transcriptomic and Ultrastructural Signatures of K+-Induced Aggregation in Phytophthora parasitica Zoospores." Microorganisms 8, no. 7 (2020): 1012. http://dx.doi.org/10.3390/microorganisms8071012.

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Most pathogenic oomycetes of the genus Phytophthora spread in water films as flagellated zoospores. Zoospores perceive and produce signals attracting other zoospores, resulting in autoaggregation in vitro or biofilm formation on plant surface. The mechanisms underlying intercellular communication and consequent attraction, adhesion and aggregation are largely unknown. In Phytophthora parasitica, the perception of a K+ gradient induces coordinated motion and aggregation. To define cellular and molecular events associated with oomycete aggregation, we combined transcriptomic and ultrastructural

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Cimminiello, C., M. Milani, T. Uberti, G. Arpaia, and G. Bonfardeci. "Effects of Ticlopidine and Indobufen on Platelet Aggregation Induced by A23187 and Adrenaline in the Presence of Different Anticoagulants." Journal of International Medical Research 17, no. 6 (1989): 514–20. http://dx.doi.org/10.1177/030006058901700603.

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As Ca2+ is known to play a fundamental role in platelet function, the effect of combining two platelet aggregating agents (adrenaline and the ionophore A23187) with different effects on Ca2+ was studied at levels subthreshold for aggregation using platelet-rich plasma from eight atherosclerotic patients. Adrenaline lowered the A23187 threshold required to induce aggregation. The effects of treating patients with the antiplatelet agents, indobufen and ticlopidine, on A23187 and adrenaline induced aggregation of platelets prepared in hirudin or sodium citrate was also evaluated. Aggregation was

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Cho, Jae Youl, David A. Fox, Vaclav Horejsi та ін. "The functional interactions between CD98, β1-integrins, and CD147 in the induction of U937 homotypic aggregation". Blood 98, № 2 (2001): 374–82. http://dx.doi.org/10.1182/blood.v98.2.374.

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CD98 is expressed on both hematopoietic and nonhematopoietic cells and has been implicated in a variety of different aspects of cell physiology and immunobiology. In this study, the functional interactions between CD98 and other adhesion molecules on the surface of the promonocyte line U937 are examined by means of a quantitative assay of cell aggregation. Several of the CD98 antibodies induced homotypic aggregation of these cells without affecting cellular viability or growth. Aggregation induced by CD98 antibodies could be distinguished from that induced by β1-integrin (CD29) ligation by lac

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