Relevant bibliographies by topics / Aggregation induced

Academic literature on the topic 'Aggregation induced'

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Published: 7 July 2024

Last updated: 7 July 2024

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Journal articles on the topic "Aggregation induced":

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 rugosin E (5 εM)-induced platelet aggregation. In thrombin (0.1 U/ml)-treated and degranulated platelets, rugosin E and ADP still caused 63.5 ± 3.0% and 61.2 ± 3.5% of platelet aggregation, respectively. Selective ADP receptor antagonists, ATP and FSBA inhibited rugosin E- and ADP-induced platelet aggregations in a concentration-dependent manner. Both rugosin E and ADP did not induce platelet aggregation in ADP (1 mM)-desensitized platelets. In contrast to ADP, rugosin E did not decrease cAMP formation in washed rabbit platelets. Both rugosin E and ADP did not cause phosphoinositide breakdown in [3H]myo-inositol-labeled rabbit platelets. In fura-2/AM- load platelets, both rugosin E and ADP induced increase in intracellular calcium concentration and these responses were inhibited by ATP and PGEj. All these data suggest that rugosin E may be an ADP receptor agonist in rabbit platelets.

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 (June 1, 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 and ATP release in normal platelet-rich plasma (PRP). This platelet aggregating factor was found in F(ab')2 fragments of the patient's IgG, which caused thromboxane B2 synthesis, elevation of cytoplasmic Ca2+ levels, and phosphorylation of 40 kDa protein in normal platelets. Platelet aggregation by the patient's IgG was inhibited by prostacyclin, dibutyryl cAMP, diltiazem, disodium ethylenediaminetetraacetate, and antimycin A plus iodoacetate, but ADP scavengers, cyclo-oxygenase inhibitors, and heparin had little or no effect. The aggregating activity of the patient's IgG absorbed to and eluted from normal platelets. The patient's Fab fragments did not induce platelet aggregation in eight of ten normal PRP but specifically inhibited aggregation induced by collagen and by the patient's IgG. The major component of an immunoprecipitate made with the patient's IgG from radiolabeled membrane proteins of normal platelet extract had a 62 kDa mol wt, while no such precipitate appeared in extracts of the patient's platelets. These results indicated that platelet aggregation by the patient's IgG was induced by the reaction of an antibody with a specific antigen on the normal platelet membrane through stimulus- response coupling. This antigen may be a collagen receptor on the platelet, most likely a polypeptide of 62 kDa under reducing condition. The defect of collagen-induced aggregation of the patient's platelets seemed to be due to alteration of the membrane protein related to this putative collagen receptor.

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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 release in normal platelet-rich plasma (PRP). This platelet aggregating factor was found in F(ab')2 fragments of the patient's IgG, which caused thromboxane B2 synthesis, elevation of cytoplasmic Ca2+ levels, and phosphorylation of 40 kDa protein in normal platelets. Platelet aggregation by the patient's IgG was inhibited by prostacyclin, dibutyryl cAMP, diltiazem, disodium ethylenediaminetetraacetate, and antimycin A plus iodoacetate, but ADP scavengers, cyclo-oxygenase inhibitors, and heparin had little or no effect. The aggregating activity of the patient's IgG absorbed to and eluted from normal platelets. The patient's Fab fragments did not induce platelet aggregation in eight of ten normal PRP but specifically inhibited aggregation induced by collagen and by the patient's IgG. The major component of an immunoprecipitate made with the patient's IgG from radiolabeled membrane proteins of normal platelet extract had a 62 kDa mol wt, while no such precipitate appeared in extracts of the patient's platelets. These results indicated that platelet aggregation by the patient's IgG was induced by the reaction of an antibody with a specific antigen on the normal platelet membrane through stimulus- response coupling. This antigen may be a collagen receptor on the platelet, most likely a polypeptide of 62 kDa under reducing condition. The defect of collagen-induced aggregation of the patient's platelets seemed to be due to alteration of the membrane protein related to this putative collagen receptor.

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 (March 1, 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 platelet aggregation induced by ristocetin, collagen, ADP, thrombin, and IgG-immune complexes. Monoclonal antibody directed against platelet glycoprotein Ib totally inhibited ristocetin-induced aggregation and release but had no effect on aggregation and release induced by the TTP sera or by any of the other platelet agonists. However, the MoAb against glycoproteins IIb/IIIa inhibited aggregation and release caused by TTP sera as well as by collagen, thrombin, and ADP but had no effect on aggregation and release induced by ristocetin. The aggregating activity could be abolished by heparin but not by the serine protease inhibitor PMSF (1 mmol/L). And although monomeric human IgG and purified Fc fragments of IgG inhibited IgG-immune complex-induced aggregation and release, they had no effect on TTP sera-induced aggregation and release nor on aggregation and release induced by any of the other agonists. Consistent with these in vitro studies showing no effect of IgG were the in vivo observations that intravenous (IV) IgG was without effect when administered to three patients with TTP. This study indicates that although a von Willebrand factor (vWF)-rich preparation of cryoprecipitate enhances the in vitro platelet aggregation and release caused by sera from the seven TTP patients we studied, the pathway of aggregation and release is not via platelet glycoprotein Ib. Also the aggregating factor of TTP sera is not neutralized in vitro or in vivo by IgG.

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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 aggregation induced by ristocetin, collagen, ADP, thrombin, and IgG-immune complexes. Monoclonal antibody directed against platelet glycoprotein Ib totally inhibited ristocetin-induced aggregation and release but had no effect on aggregation and release induced by the TTP sera or by any of the other platelet agonists. However, the MoAb against glycoproteins IIb/IIIa inhibited aggregation and release caused by TTP sera as well as by collagen, thrombin, and ADP but had no effect on aggregation and release induced by ristocetin. The aggregating activity could be abolished by heparin but not by the serine protease inhibitor PMSF (1 mmol/L). And although monomeric human IgG and purified Fc fragments of IgG inhibited IgG-immune complex-induced aggregation and release, they had no effect on TTP sera-induced aggregation and release nor on aggregation and release induced by any of the other agonists. Consistent with these in vitro studies showing no effect of IgG were the in vivo observations that intravenous (IV) IgG was without effect when administered to three patients with TTP. This study indicates that although a von Willebrand factor (vWF)-rich preparation of cryoprecipitate enhances the in vitro platelet aggregation and release caused by sera from the seven TTP patients we studied, the pathway of aggregation and release is not via platelet glycoprotein Ib. Also the aggregating factor of TTP sera is not neutralized in vitro or in vivo by IgG.

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-like enzymes was correlated with their effectiveness on the retractility and elasticity of the clots. Platelet aggregation induced by thrombin or thrombocytin could be inhibited by heparin with antithrombin III while that by acutin or batroxobin could not. Indomethacin showed weak inhibition on the aggregation while the ADP-scavenging system, creatine phosphate/creatine phosphokinase, inhibited the aggregation induced by the three thrombin-like enzymes but not that by thrombin. Platelet aggregation induced by the thrombin-like enzymes could not be inhibited by PAF antagonists-BN 52021, kadsurenone or L-652,731. In the presence of EGTA, only thrombin could induce ATP release from platelets. Thrombin-like enzymes and low concentration of thrombin did not form thromboxane B2. Nitroprusside and prostaglandin E1 completely inhibited the aggregation, mepacrine and imipramine showed marked inhibition while verapamil had only weak inhibition. It is concluded that the aggregation induced by the thrombin-like enzymes is different from that of thrombin and mainly due to ADP released from platelets.

YAGER, RONALD R. "CHOQUET AGGREGATION USING ORDER INDUCING VARIABLES." International Journal of Uncertainty, Fuzziness and Knowledge-Based Systems 12, no. 01 (February 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 in nearest neighbor methods. We also consider the Choquet aggregation of complex objects such as matrices and vectors.

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 (November 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 also studied using platelets resuspended in Ca2+-free and Ca2+-enriched Tyrode solution. Before treatment hirudin treated platelet-rich plasma, which has physiological extraplatelet Ca2+ levels, was more sensitive to A23187 and adrenaline than was citrated platelet-rich plasma, which has suppressed Ca2+ levels. Ticlopidine significantly raised the concentration of A23187 required to induce aggregation in citrated but not hirudin treated platelet-rich plasma. Indobufen did not significantly affect A23187 induced aggregation. Ticlopidine acts by inhibiting the glycoprotein IIb – IIIa complex on the platelet membranes. Low levels of extracellular Ca2+ and ticlopidine may act synergistically to reduce the aggregatory response of stimulated platelets.

Tang, B., Z. Zhao, Z. Wang, P. Lu, C. Chan, D. Liu, J. Lam, H. Sung, I. Williams, and Y. Ma. "Aggregation-Induced Emission." Synfacts 2009, no. 12 (November 20, 2009): 1345. http://dx.doi.org/10.1055/s-0029-1218183.

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

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Dissertations / Theses on the topic "Aggregation induced":

Klebensberger, Janosch. "Detergent-induced cell aggregation in Pseudomonas aeruginosa." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:352-opus-26614.

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Östman, Johan. "Mechanisms involved in amyloid induced cytotoxicity." Doctoral thesis, Umeå universitet, Molekylärbiologi (Teknat- och Medfak), 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-541.

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Amyloidoses comprise a group of diseases where normal or mutated protein precipitates into amyloid fibrils. The deposition of fibrils causes dysfunction of organs and toxicity to nervous tissue. Up to date, 24 different proteins and peptides are known to be able to form amyloid fibrils. The most well known are Amyloid beta peptide and Prione protein causing Alzheimer’s disease and Creutzfeld Jacob’s disease respectively. The aims of this thesis were to investigate the structural properties of cytotoxic amyloid and examine the mechanisms involved. The model protein mostly used in the studies was the plasma protein transthyretin (TTR). Familial Amyloidotic Polyneuropathy (FAP) is a hereditary, autosomal-dominant neurodegenerative disease caused by point mutations in the TTR gene. One of the most common variants of FAP is a mutation in position 30 where alanine is exchanged for methonine. This gives rise to “Skellefteåsjukan” in Sweden. TTR is secreted into the plasma as a tetramer. Point mutations destabilize the tetramer leading to disassembled monomers, which undergo partial denaturation as an initiation step to aggregation and amyloid fibril formation. In vivo amyloidogenesis takes a long time and does not occur until late in adult life. Most of the clinical TTR mutations do not form amyloid in vitro under physiological conditions. We have created amyloidogenic TTR mutants that are prone to aggregate and form fibrils under physiological conditions. This provides us with a model system on the cellular level for studies of the mechanisms of amyloid associated cytotoxicity as we can control the aggregation process and capture defined stages in the TTR amyloidogenic pathway. We used Atomic Force Microscopy (AFM) to follow the morphology of aggregates during fibril formation. Initially, amorphous aggregates were formed that subsequently matured into fibrillar structures, denoted protofilaments. This observation was interpreted as an optimisation of ß-strand registers. In addition we identified a correlation between the presence of early-formed aggregates of TTR and cytotoxicity. The toxic response was mediated via an apoptotic mechanism. We were not able to more carefully determine the structure and size of the toxic TTR species. To address this problem we turned to another amyloidogenic protein, equine lysozyme (EL). Intermediate samples corresponding to the aggregation and growth phase of amyloid fibrils of EL were collected. These samples were subjected to cytotoxicity assays as well as monomeric starting material and mature amyloid fibrillar species. The results clearly showed that the soluble oligomers were cytotoxic in contrast to the monomers and fibrils. Our data indicate that the toxic properties of the oligomers are size dependent. In this thesis we asked the question whether all mutated forms of TTR can be expressed and secreted or if there is a selection against the most aggressive mutations in vivo? We transfected hematopoetic K562 cells with wild type or mutant TTR, with or without the N-terminal signal peptide, responsible for secretion, to generate both extra- and intracellular TTR. We show that the post-translational quality control of the cells does not allow intracellular mutant TTR outside the secretory pathway, possibly due to the cytotoxic effects, while translocated to the secretory pathway made it escape the quality control permitting secretion and amyloid formation outside the cells. We have further analyzed the cytotoxic mechanisms induced by TTR oligomers with a focus on intracellular apoptotic signalling pathways. We show that TTR oligomers bind to the surface of the target cells but are not taken up, that is in contrast to mature fibrils that do not bind them at all. The apoptotic response occurred in a caspase-independent and a free radical dependent way.

Menzen, Tim Andreas. "Temperature-induced unfolding, aggregation, and interaction of therapeutic monoclonal antibodies." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-175200.

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Nyström, Roger. "Aggregation of calcium carbonate dispersions induced by electrolytes and polyelectrolytes /." Åbo : Åbo akademi University, 2004. http://catalogue.bnf.fr/ark:/12148/cb40124838x.

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Knight, Grady C. "The molecular chaperone α-crystallin protects proteins from UV-induced aggregation." Diss., Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/30486.

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Xu, Meisheng. "The field-induced aggregation and magneto-optical properties in magnetic fluids." Thesis, London South Bank University, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300592.

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Dong, Yujie. "Synthesis, photophysical properties and applications of aggregation-induced emission materials based on cyanostilbene moiety." HKBU Institutional Repository, 2016. https://repository.hkbu.edu.hk/etd_oa/313.

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The concept of "aggregation-induced emission" (AIE) effect has induced a great deal of attention these days. Now, exploration of new AIE-active molecular system and multiple high technique applications for AIE materials are the two research hotspots. Cyanostilbene, as a classical structural unit in photoelectric functional materials, also exhibited this unique luminescence behavior. The research background was illustrated in Chapter 1, which mainly introduced the development of this subject. In this project, Chapter 2 and Chapter 3 presented two classes of functionalized AIE-active molecules based on cyanostilbene moiety, and their applications were investigated, while Chapter 4 demonstrated a series of donor-acceptor (D-A) molecules with highly emissive unit, and their photophysical properties were studied.;In Chapter 2, four different donor-substituted cyanostilbene-based dipyrrins were synthesized and characterized. The investigation of photophysical properties confirms that these molecules are AIE-active, which should be attributed to the cyanostilbene moiety. The introduction of different donor groups showed little impact on their luminescence. Furthermore, the emission properties of these molecules were found to be sensitive to Zn2+, that is, addition of Zn2+ enormously enhanced its fluorescence in THF. The titration experiments proved they showed good selectivity and sensitivity for Zn2+ detection with relatively low limit of detection. Job's curve and spectral studies of their corresponding zinc complex indicated that the ratio for dipyrrins and Zn2+ is 2:1, which suggested the formation of zinc complex by chelation-enhanced fluorescence (CHEF) effect should be the reason of the enhanced fluorescence. By combining dipyrrin with typical AIE-active moiety tetraphenylethylene (TPE), an AIE-active TPE-based dipyrrin was prepared. The studies of its fluorogenic Zn2+ detection confirmed that the CHEF effect together with AIE effect are responsible for the intense fluorescence, indicating the potential application as a Zn2+ detector in aqueous media.;In Chapter 3, the cyanostilbene backbone was functionalized with a terpyridine unit to construct four terpyridine-based cyanostilbene molecules with different donor substitutents. The investigation of their photophysical properties confirms that they are AIEE-active. With the effect of different electron-donating groups, their solid-state fluorescence color was adjusted from blue to orange-red successfully. According to the calculation results of their frontier molecular orbitals, terpyridine has little impacts on their luminescence, but would influence their solid-state emission obviously owing to its large steric hindrance. This class of molecules displayed higher luminescence efficiency in solid state than in their dissolved state. The twisted molecular conformation in single crystal, which effectively avoids close π-π stacking, was assumed to be responsible for the high luminescence efficiency in solid state. This kind of molecules show distinct switched fluorescence by stimuli of acid/base vapors, and this phenomenon derives from the protonation effect of nitrogen atoms in the terpyridine unit. Moreover, three of these molecules exhibit good electroluminescence properties. Especially, the crystal of non-donor substituted molecule show amplified spontaneous emission (ASE) properties, indicating this blue-emissive material can be used in multiple areas such as chemical sensor, organic light emitting diodes (OLEDs) and organic laser media.

Yu, Wai Hong. "Synthesis, Characterization and application studies of new aggregation-induced emission (AIE)-active materials." HKBU Institutional Repository, 2018. https://repository.hkbu.edu.hk/etd_oa/496.

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The structural design, synthesis and characterization of luminogens with aggregation-induced emission (AIE) properties are studied in this thesis. The remarkable emission properties, thermal stability and biocompatibility of the AIE-active materials demonstrate the promising applications in bioimaging and organic light-emitting diodes (OLEDs).;Chapter 1 introduces the existence of aggregation-caused quenching (ACQ) effect in most conventional organic dyes as well as phosphorescent transitional metal complexes. Discovery of AIE and its mechanical study allow further exploration of usage in organic luminescent materials. This chapter also gives some examples and the applications these AIE-active compounds.;In Chapter 2, a series of cyanostilbenes with simple electron donor (D)-p-electron acceptor (A) structure are presented and synthesized. They exhibit remarkable AIE effect as well as deep red emission peak in 95 % water fraction in THF. These results indicate that attachment of these electron acceptors provides alternative strategy for designing highly emissive AIE-active materials.;In Chapter 3, strongly emissive cyanostilbenes with phenothiazine unit are designed and synthesized. This chapter also investigates the effect of substituents in phenothiazine and terminal cyanostilbene on the photophysical properties and AIE effect. The results suggest that they are AIE-active with different sizes in nano-aggregates. Furthermore, these dyes exhibit clear and strong fluorescence in live cell imaging with excellent biocompatibility.;In Chapter 4, a series of AIE-active phosphorescent Pt(II) complexes made up of C^N^C tridentate ligands are designed and synthesized. They exhibit different morphologies and emission properties upon aggregation in 90 % water in acetonitrile although similar tridentate ligands are applied. One of the complexes in this chapter show nano-rod formation with the highest quantum efficiency in aggregated state, suggesting that rapid self-assembly process occurs to prevent non-radiative decay and oxygen quenching.;In Chapter 5, a series of bis-cyanostyryl fluorophores are designed and synthesized. They are emissive in solid state with colour range from orange to NIR region. Furthermore, they are AIE-active and some of them may contain hybridized local and charge transfer (HLCT) excited state to achieve highly efficient emission upon solvatochromic investigation. Some bis-cyanostyryl thiophenes are fabricated in OLED devices show deep-red to NIR emission, indicative of a promising way to design solid-state NIR-emissive compounds using bis-cyanostyryl derivatives.;Finally, Chapter 6 and 7 present the concluding remarks and the experimental details of the work in Chapters 2 to 5, respectively.

Brummitt, Rebecca K. "Urea-induced dissociation of non-native aggregates of alpha-Chymotrypsinogen A kinetics, thermodynamics, and competing pathways /." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 103 p, 2008. http://proquest.umi.com/pqdweb?did=1597632641&sid=12&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Photchanachai, Songsin. "Studies on Molecular Aggregation and Degradation of Food Proteins Induced by High-Temperature Treatments." Kyoto University, 2003. http://hdl.handle.net/2433/148327.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第10507号
農博第1380号
新制||農||882(附属図書館)
学位論文||H15||N3862(農学部図書室)
UT51-2003-U477
京都大学大学院農学研究科応用生命科学専攻
(主査)教授北畠直文, 教授小川正, 教授吉川正明
学位規則第4条第1項該当

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Books on the topic "Aggregation induced":

Tang, Youhong, and Ben Zhong Tang, eds. Aggregation-Induced Emission. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-89933-2.

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Qin, Anjun, and Ben Zhong Tang, eds. Aggregation-Induced Emission: Fundamentals. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.

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Tang, Ben Zhong, and Anjun Qin. Aggregation-induced emission: Fundamentals. Chichester, West Sussex, United Kingdom: John Wiley & Sons Inc., 2014.

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Tang, Youhong, and Ben Zhong Tang, eds. Principles and Applications of Aggregation-Induced Emission. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99037-8.

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Fujiki, Michiya, Bin Liu, and Ben Zhong Tang, eds. Aggregation-Induced Emission: Materials and Applications Volume 1. Washington, DC: American Chemical Society, 2016. http://dx.doi.org/10.1021/bk-2016-1226.

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Fujiki, Michiya, Bin Liu, and Ben Zhong Tang, eds. Aggregation-Induced Emission: Materials and Applications Volume 2. Washington, DC: American Chemical Society, 2016. http://dx.doi.org/10.1021/bk-2016-1227.

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Husband, J. C. Shear-induced aggregationof carboxylated polymer lattices. Manchester: UMIST, 1993.

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Cheung, Albert. Pax3 and PAX3/FKHR induces cell aggregation and morphogenic mesenchymal-epithelial transition. Ottawa: National Library of Canada, 2002.

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Zhong Tang, Ben, and Xinggui Gu, eds. Aggregation-Induced Emission. De Gruyter, 2022. http://dx.doi.org/10.1515/9783110672220.

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Zhong Tang, Ben, and Xinggui Gu, eds. Aggregation-Induced Emission. De Gruyter, 2022. http://dx.doi.org/10.1515/9783110673074.

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Book chapters on the topic "Aggregation induced":

Beysens, Daniel, Coggio Houessou, and Françoise Perrot. "Wetting Induced Aggregation." In On Growth and Form, 211–17. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-5165-5_15.

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Dong, Yongqiang. "Crystallization-Induced Emission Enhancement." In Aggregation-Induced Emission: Fundamentals, 323–35. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.ch15.

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Corey, Joyce Y. "Synthesis of Siloles (and Germoles) that Exhibit the AIE Effect." In Aggregation-Induced Emission: Fundamentals, 1–37. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.ch01.

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Mullin, Jerome L., and Henry J. Tracy. "Aggregation-Induced Emission in Group 14 Metalloles (Siloles, Germoles, and Stannoles): Spectroscopic Considerations, Substituent Effects, and Applications." In Aggregation-Induced Emission: Fundamentals, 39–60. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.ch02.

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Xu, Bin, Jibo Zhang, and Wenjing Tian. "Aggregation-Induced Emission of 9,10-Distyrylanthracene Derivatives and Their Applications." In Aggregation-Induced Emission: Fundamentals, 61–82. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.ch03.

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Shimizu, Masaki. "Diaminobenzene-Cored Fluorophores Exhibiting Highly Efficient Solid-State Luminescence." In Aggregation-Induced Emission: Fundamentals, 83–104. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.ch04.

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Fery-Forgues, Suzanne. "Aggregation-Induced Emission in Organic Ion Pairs." In Aggregation-Induced Emission: Fundamentals, 105–25. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.ch05.

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Huang, Jing, Qianqian Li, and Zhen Li. "Aggregation-Induced Emission Materials: the Art of Conjugation and Rotation." In Aggregation-Induced Emission: Fundamentals, 127–53. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.ch06.

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Yuan Shen, Xiao, Anjun Qin, and Jing Zhi Sun. "Red-Emitting AIE Materials." In Aggregation-Induced Emission: Fundamentals, 155–67. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.ch07.

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Hua, Jianli, He Tian, and Hao Zhang. "Properties of Triarylamine Derivatives with AIE and Large Two-Photon Absorbing Cross-Sections." In Aggregation-Induced Emission: Fundamentals, 169–84. Chichester, United Kingdom: John Wiley and Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118735183.ch08.

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Conference papers on the topic "Aggregation induced":

Dong, Yongqiang, Jacky Wing Yip Lam, Anjun Qin, Zhen Li, Jiaxin Sun, Hoi Sing Kwok, and Ben Zhong Tang. "Aggregation-induced emission." In SPIE Optics + Photonics, edited by Zakya H. Kafafi and Franky So. SPIE, 2006. http://dx.doi.org/10.1117/12.679373.

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Teng, C. M., and F. N. Ko. "COMPARISON OF THE PLATELET AGGREGATION INDUCED BY THREE THROMBIN-LIKE ENZYMES OF SNAKE VENOMS AND THROMBIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644535.

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Acutin was isolated from Agkistrodon acutus venom and batroxobin and thrombocytin were isolated from Bothrops atrox venom. These three thrombin-like enzymes had different specificity for platelet activation and fibrinogen clotting. The clotting activities were 700, 170 and 7 μ/mg for batroxobin, acutin and thrombocytin, respectively. They induced aggregation and ATP release of washed rabbit platelets. The aggregating activities were 102, 104 and 105 times less than that of thrombin for thrombocytin, acutin and batroxobin, respectively basing on the clotting unit. The platelet -activating potency was correlated with their effectiveness on the retractility and elasticity of the clots. Platelet aggregation induced by thrombin or thrombocytin could be inhibited by heparin with antithrombin III while that by acutin or batroxobin could not. The thrombin-like enzymes did not induce aggregation of thrombin-degranulated platelets even fibrinogen was added. Indomethacin showed weak inhibition on the aggregation while the ADP - scavenging system, creatine phosphate/creatine phosphokinase, or apyrase inhibited the aggregation induced by the three thrombin-like enzymes but not that by thrombin. In the presence of EGTA, only thrombin could induce ATP release from platelets. It is concluded that the aggregation induced by thrombin-like enzymes is different from that of thrombin and mainly due to ADP released from platelets.

Pei, Daowu, Yuying Shan, and Huanzhang Liu. "On consistent induced matrix aggregation operators." In 2013 Joint IFSA World Congress and NAFIPS Annual Meeting (IFSA/NAFIPS). IEEE, 2013. http://dx.doi.org/10.1109/ifsa-nafips.2013.6608541.

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Hong, Yuning, Yongqiang Dong, Hui Tong, Zhen Li, Matthias Häußler, Jacky Wing Yip Lam, and Ben Zhong Tang. "Aggregation- and crystallization-induced light emission." In Integrated Optoelectronic Devices 2007, edited by James G. Grote, Francois Kajzar, and Nakjoong Kim. SPIE, 2007. http://dx.doi.org/10.1117/12.707609.

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Nagata, H., S. Nomura, K. Oda, T. Kokawa, and K. Yasunaga. "ANALYSIS OF THE FUNCTIONAL ROLE OF PLATELET MEMBRANE GLYCOPROTEINS WITH MONOCLONAL ANTIBODIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643509.

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Eight monoclonal antibodies were obtained which recognized platelet surface antigens of these, 5 (NNKYl-32, NNKY2-5, NNKY2-6, NNKY2-11, NNKY2-18 ) recognized GP IIb-IIIa complex, 2 (NNKY5-4, NNKY5-5 ) recognized GP lb and 1 (NNKYl-19) recognized CD 9 antigen. They were used to research the platelet membrane antigens.Monoclonal antibodies that recognize CD 9 antigen, which exists on the surface of platelets, acute lymphoblastic leukemia cells, eosinophils and other tissue, are known to act as an aggregating agent to platelets and NNKYl-19 was fond to induce platelet aggregation accompanied by ATP release. NNKY5-4 had no effect on platelet functions. NNKY5-5 inhibited aggregation induced by ristocetin but had no effect on aggregation induced by ADP, collagen, thrombin, and NNKYl-19. NNKYl-32, 2-5, 2-6, 2-11, and 2-18 inhibited aggregation induced by ADP, collagen, thrombin, and NNKYl-19, although slight release of ATP was recognized when NNKYl-19-induced aggregation was completely inhibited by NNKYl-32. Mutual inhibition of binding to platelet membranes between the 3 groups of monoclonal antibodies was not recognizedNNKYl-19-induced aggregation was associated with a lag time that was plo-longed in inverse proportion to antibody concentration. Aspirin had almost no effect on NNKYl-19-induced aggregation. A TXA2 receptor antagonist, a calci-um-channel blocking drug and EDTA inhibited NNKYl-19-induced aggregation. These results indicate that GP I b, GP IIb-IIIa complex and the cyclooxygenase pathway are not involved in NNKYl-19-induced platelet activation, that the target of NNKYl-19 on the platelet membrane is same as that of TXA2, and that the mechanism of activation by NNKYl-19 is related to calcium flux.

Patel, R., and R. Bick. "PLATELET DYSFUNCTION INDUCED BY TETRAHYDROCANNABINOL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644877.

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Many drugs and other agents have been reported to induce platelet dysfunction and clinical bleedability; however, tetrahydrocannabinol (marijuana) has thus far not been reported. The patient herein described is a 28-year-old Caucasian female who wasreferred for evaluation of easy and spontaneous bruising. On history, the patient related that for a three-month period she had been developing spontaneous ecchymoses of the extremities and torso. She denied any medication other than heavy marijuana use. Hemostasis evaluation revealed her to have a normal prothrombin time, partial thromboplastin time (PTT), Factor VIII coagulant activity (Factor VIII:C), Factor VIII related antigen (Factor VIII:RAg), and ristocetincofactor activity. Platelet aggregation was performed which revealed abnormal aggregation to epinephrine, adenosine diphosphate (ADP) and abnormal release but normal aggregation toristocetin. She was asked to refrainfrom marijuana and was reaggregated revealing normal aggregation and release to epinephrine, ADP, collagen and arachidonic acid; however, ADP release induced by ristocetin remainedmoderately abnormal, even though aggregation was normal. In addition, with cessation of marijuana use, her clinical bruising abated.Following this, she again indulged in marijuana and she was reaggregated, revealing delayed aggregation and release to epinephrine with abnormal aggregation to ADP. Additionally, ristocetin release and adenosine triphosphate (ATP) release remained abnormal but aggregation remained normal and arachidonic acid aggregationremained normal.In summary, we herein describe a young female who demonstrated aggregation abnormalities and clinically significant spontaneous bruising during periods of using marijuana; the defect disappeared upon cessation of marijuana and reappeared upon resumption of marijuana use. The defect atpresent appears to be that of a membrane-type defect with no evidence that marijuana interferes with the prostaglandin pathway.

Modderman, P. W., J. G. Huisman, J. A. van Mourik, A. E. G. Kr, and v. d. Borne. "PLATELET ACTIVATION INDUCED BY A MONOCLONAL ANTIBODY AGAINST THE PLATELET GP Ilb/IIIa COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643514.

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A receptor for fibrinogen on the platelet GP Ila/lIIb complex is induced by ADP, thrombin and other agonists. To study functional domains on GP Ilb/IIIa, the effects of anti-GP Ilb/IIIa monoclonal antibodies (Mab’s) on platelet function were determined. One of these Mab’s, 6C9, induced platelet aggregation. The antibody binds to the intact GP Ilb/IIIa complex only, not to free GP lib or free GP Ilia. Its epitope is different from that of C17, a Mab that inhibits ADP-induced fibrinogen binding and platelet aggregation. 6C9 induces fibrinogen-mediated aggregation rather than agglutination since 6C9-induced platelet interactions were blocked by treatments that also inhibited the effects of ADP etc., without inhibiting binding of 6C9 itself. 6C9 induces binding of 125I-fibrinogen (35.000 ± 7.300 molecules/platelet, Kd = 1.3 ± 0.4 µM) to unstirred platelets. Binding of fibrinogen was 60 to 80% inhibited by apyrase, which indicates that 6C9-induced fibrinogen binding is largely mediated via ADP released from platelets. In addition, 6C9 induced aggregation of platelets in the absence of extracellular fibrinogen. Mediation of this process by platelet fibrinogen or other a-granule proteins, released upon activation by 6C9, was implicated by the finding that aggregation of washed platelets, but not of platelets to which fibrinogen was added, could be blocked by PGI2. Platelet release was also assessed directly by measuring β-thromboglobulin (α-granules) and (14C) serotonin (dense granules) in the medium of unstirred platelets incubated with 6C9. F(ab')2 fragments of 6C9 only aggregated platelets in the presence of fibrinogen and did not release (14C) serotonin. Moreover, release induced by intact 6C9 was inhibited by anti-GP Ilb/IIIa Mab C17 but not by C17 F(ab’)2, although the latter inhibited ADP-induced platelet aggregation. These data indicate that binding of antibodies to specific sites on GP Ilb/IIIa may induce Fc-dependent platelet activation.This study was supported by the Foundation for Medical Research MEDIGON (grant no. 900-526-057.

Jumat, Saidatul Aisyah Haji, Nur Basirah Mohd Addie Sukaimi, Malai Haniti Sheikh Abdul Hamid, Ying Woan Soon, and Anwar Usman. "Aggregation-induced emission properties of trans-stilbene." In THE 5TH INTERNATIONAL TROPICAL RENEWABLE ENERGY CONFERENCE (THE 5TH iTREC). AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0063770.

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Williams, Stuart J., Aloke Kumar, and Steven T. Wereley. "Optically Induced Electrohydrodynamics and Electrokinetic Colloidal Aggregation." In ASME 2009 Fluids Engineering Division Summer Meeting. ASMEDC, 2009. http://dx.doi.org/10.1115/fedsm2009-78121.

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Recently, we have demonstrated a novel optically induced AC electrokinetic technique that rapidly, continuously and selectively concentrates micro and nanoparticles on an electrode surface [1–3]. This is demonstrated with a highly focused near-infrared (1,064 nm) laser beam applied to parallel plate electrodes separated by 50 μm without the need for photosensitive materials. This dynamic optically-induced technique can be applied towards a variety of lab-on-a-chip applications. This paper will explain the fundamental physical mechanisms involved, necessary in order to replicate and implement this technique. This dynamic fluid and particle manipulation technique may prove valuable to a variety of applications in micro- and nanotechnology.

Alfaro-Garcia, Victor G., Anna M. Gil-Lafuente, and Jose M. Merigo. "Induced generalized ordered weighted logarithmic aggregation operators." In 2016 IEEE Symposium Series on Computational Intelligence (SSCI). IEEE, 2016. http://dx.doi.org/10.1109/ssci.2016.7850012.

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Reports on the topic "Aggregation induced":

Petrova, I. V., O. A. Trubacheva, O. S. Mangataeva, T. E. Suslova, I. V. Kovalev, and S. V. Gusakova. INFLUENCE OF HYDROGEN SULFIDE ON COLLAGEN-INDUCED AGGREGATION OF HUMAN PLATELETS. DOI CODE, 2015. http://dx.doi.org/10.18411/doicode-2023.141.

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Chefetz, Benny, Baoshan Xing, Leor Eshed-Williams, Tamara Polubesova, and Jason Unrine. DOM affected behavior of manufactured nanoparticles in soil-plant system. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604286.bard.

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The overall goal of this project was to elucidate the role of dissolved organic matter (DOM) in soil retention, bioavailability and plant uptake of silver and cerium oxide NPs. The environmental risks of manufactured nanoparticles (NPs) are attracting increasing attention from both industrial and scientific communities. These NPs have shown to be taken-up, translocated and bio- accumulated in plant edible parts. However, very little is known about the behavior of NPs in soil-plant system as affected by dissolved organic matter (DOM). Thus DOM effect on NPs behavior is critical to assessing the environmental fate and risks related to NP exposure. Carbon-based nanomaterials embedded with metal NPs demonstrate a great potential to serve as catalyst and disinfectors. Hence, synthesis of novel carbon-based nanocomposites and testing them in the environmentally relevant conditions (particularly in the DOM presence) is important for their implementation in water purification. Sorption of DOM on Ag-Ag₂S NPs, CeO₂ NPs and synthesized Ag-Fe₃O₄-carbon nanotubebifunctional composite has been studied. High DOM concentration (50mg/L) decreased the adsorptive and catalytic efficiencies of all synthesized NPs. Recyclable Ag-Fe₃O₄-carbon nanotube composite exhibited excellent catalytic and anti-bacterial action, providing complete reduction of common pollutants and inactivating gram-negative and gram-positive bacteria at environmentally relevant DOM concentrations (5-10 mg/L). Our composite material may be suitable for water purification ranging from natural to the industrial waste effluents. We also examined the role of maize (Zeamays L.)-derived root exudates (a form of DOM) and their components on the aggregation and dissolution of CuONPs in the rhizosphere. Root exudates (RE) significantly inhibited the aggregation of CuONPs regardless of ionic strength and electrolyte type. With RE, the critical coagulation concentration of CuONPs in NaCl shifted from 30 to 125 mM and the value in CaCl₂ shifted from 4 to 20 mM. This inhibition was correlated with molecular weight (MW) of RE fractions. Higher MW fraction (> 10 kDa) reduced the aggregation most. RE also significantly promoted the dissolution of CuONPs and lower MW fraction (< 3 kDa) RE mainly contributed to this process. Also, Cu accumulation in plant root tissues was significantly enhanced by RE. This study provides useful insights into the interactions between RE and CuONPs, which is of significance for the safe use of CuONPs-based antimicrobial products in agricultural production. Wheat root exudates (RE) had high reducing ability to convert Ag+ to nAg under light exposure. Photo-induced reduction of Ag+ to nAg in pristine RE was mainly attributed to the 0-3 kDa fraction. Quantification of the silver species change over time suggested that Cl⁻ played an important role in photoconversion of Ag+ to nAg through the formation and redox cycling of photoreactiveAgCl. Potential electron donors for the photoreduction of Ag+ were identified to be reducing sugars and organic acids of low MW. Meanwhile, the stabilization of the formed particles was controlled by both low (0-3 kDa) and high (>3 kDa) MW molecules. This work provides new information for the formation mechanism of metal nanoparticles mediated by RE, which may further our understanding of the biogeochemical cycling and toxicity of heavy metal ions in agricultural and environmental systems. Copper sulfide nanoparticles (CuSNPs) at 1:1 and 1:4 ratios of Cu and S were synthesized, and their respective antifungal efficacy was evaluated against the pathogenic activity of Gibberellafujikuroi(Bakanae disease) in rice (Oryza sativa). In a 2-d in vitro study, CuS decreased G. fujikuroiColony- Forming Units (CFU) compared to controls. In a greenhouse study, treating with CuSNPs at 50 mg/L at the seed stage significantly decreased disease incidence on rice while the commercial Cu-based pesticide Kocide 3000 had no impact on disease. Foliar-applied CuONPs and CuS (1:1) NPs decreased disease incidence by 30.0 and 32.5%, respectively, which outperformed CuS (1:4) NPs (15%) and Kocide 3000 (12.5%). CuS (1:4) NPs also modulated the shoot salicylic acid (SA) and Jasmonic acid (JA) production to enhance the plant defense mechanisms against G. fujikuroiinfection. These results are useful for improving the delivery efficiency of agrichemicals via nano-enabled strategies while minimizing their environmental impact, and advance our understanding of the defense mechanisms triggered by the NPs presence in plants.

Naim, Michael, Andrew Spielman, Shlomo Nir, and Ann Noble. Bitter Taste Transduction: Cellular Pathways, Inhibition and Implications for Human Acceptance of Agricultural Food Products. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7695839.bard.

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Historically, the aversive response of humans and other mammals to bitter-taste substances has been useful for survival, since many toxic constituents taste bitter. Today, the range of foods available is more diverse. Many bitter foods are not only safe for consumption but contain bitter constituents that provide nutritional benefits. Despite this, these foods are often eliminated from our current diets because of their unacceptable bitterness. Extensive technology has been developed to remove or mask bitterness in foods, but a lack of understanding of the mechanisms of bitterness perception at the taste receptor level has prevented the development of inhibitors or efficient methods for reducing bitterness. In our original application we proposed to: (a) investigate the time course and effect of selected bitter tastants relevant to agricultural products on the formation of intracellular signal molecules (cAMP, IP3, Ca2+) in intact taste cells, in model cells and in membranes derived therefrom; (b) study the effect of specific bitter taste inhibitors on messenger formation and identify G-proteins that may be involved in tastant-induced bitter sensation; (c) investigate interactions and self-aggregation of bitter tastants within membranes; (d) study human sensory responses over time to these bitter-taste stimuli and inhibitors in order to validate the biochemical data. Quench-flow module (QFM) and fast pipetting system (FPS) allowed us to monitor fast release of the aforementioned signal molecules (cGMP, as a putative initial signal was substituted for Ca2+ ions) - using taste membranes and intact taste cells in a time range below 500 ms (real time of taste sensation) - in response to bitter-taste stimulation. Limonin (citrus) and catechin (wine) were found to reduce cellular cAMP and increase IP3 contents. Naringin (citrus) stimulated an IP3 increase whereas the cheese-derived bitter peptide cyclo(leu-Trp) reduced IP3 but significantly increased cAMP levels. Thus, specific transduction pathways were identified, the results support the notion of multiple transduction pathways for bitter taste and cross-talk between a few of those transduction pathways. Furthermore, amphipathic tastants permeate rapidly (within seconds) into liposomes and taste cells suggesting their availability for direct activation of signal transduction components by means of receptor-independent mechanisms within the time course of taste sensation. The activation of pigment movement and transduction pathways in frog melanophores by these tastants supports such mechanisms. Some bitter tastants, due to their amphipathic properties, permeated (or interacted with) into a bitter tastant inhibitor (specific phospholipid mixture) which apparently forms micelles. Thus, a mechanism via which this bitter taste inhibitor acts is proposed. Human sensory evaluation experiments humans performed according to their 6-n-propyl thiouracil (PROP) status (non-tasters, tasters, super-tasters), indicated differential perception of bitterness threshold and intensity of these bitter compounds by different individuals independent of PROP status. This suggests that natural products containing bitter compounds (e.g., naringin and limonin in citrus), are perceived very differently, and are in line with multiple transduction pathways suggested in the biochemical experiments. This project provides the first comprehensive effort to explore the molecular basis of bitter taste at the taste-cell level induced by economically important and agriculturally relevant food products. The findings, proposing a mechanism for bitter-taste inhibition by a bitter taste inhibitor (made up of food components) pave the way for the development of new, and perhaps more potent bitter-taste inhibitors which may eventually become economically relevant.

Axenrot, Thomas, Erik Degerman, and Anders Asp. Seasonal variation in thermal habitat volume for cold-water fish populations : implications for hydroacoustic survey design and stock assessment. Department of Aquatic Resources, Swedish University of Agricultural Sciences, 2023. http://dx.doi.org/10.54612/a.5i05rb1iu1.

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For accurate stock assessment, survey design must consider fish behavior and ecology. Yearlings and older individuals of the commercially exploited cold-water species vendace (Coregonus albula) are found below the metalimnion through periods of thermal stratification. These stratification periods generally last for 3-4 months, from the middle of summer to early autumn. In lakes with heterogeneous distribution of depths, the habitat volume for vendace vary drastically within and across years, which affects the distribution and population densities. Variable thermal habitat volumes, with food and oxygen depletion in the hypolimnion through the period of stratification, may act as a population size-regulating factor. Using hydroacoustics in combination with trawl data and temperature profiles, we examined the distribution of vendace through annual periods of thermal stratification. We found that yearling and older vendace these periods were confined to cold-water habitat volumes representing less than 10 % of the total water volume of Lake Mälaren, the third largest lake in Sweden. By introducing stratification to the design of hydroacoustic surveys supported by midwater trawling, seasonal aggregations of fish in temporally restricted thermal habitat volumes can be used to lower survey effort and improve the precision in estimates of population size. Temporally restricted habitat volumes may induce risks for the populations to over-fishing and sensitivity to environmental changes that potentially may call for directed management.

Hertel, Thomas, David Hummels, Maros Ivanic, and Roman Keeney. How Confident Can We Be in CGE-Based Assessments of Free Trade Agreements? GTAP Working Paper, June 2003. http://dx.doi.org/10.21642/gtap.wp26.

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With the proliferation of Free Trade Agreements (FTAs) over the past decade, demand for quantitative analysis of their likely impacts has surged. The main quantitative tool for performing such analysis is Computable General Equilibrium (CGE) modeling. Yet these models have been widely criticized for performing poorly (Kehoe, 2002) and having weak econometric foundations (McKitrick, 1998; Jorgenson, 1984). FTA results have been shown to be particularly sensitive to the trade elasticities, with small trade elasticities generating large terms of trade effects and relatively modest efficiency gains, whereas large trade elasticities lead to the opposite result. Critics are understandably wary of results being determined largely by the authors’ choice of trade elasticities. Where do these trade elasticities come from? CGE modelers typically draw these elasticities from econometric work that uses time series price variation to identify an elasticity of substitution between domestic goods and composite imports (Alaouze, 1977; Alaouze, et al., 1977; Stern et al., 1976; Gallaway, McDaniel and Rivera, 2003). This approach has three problems: the use of point estimates as “truth”, the magnitude of the point estimates, and estimating the relevant elasticity. First, modelers take point estimates drawn from the econometric literature, while ignoring the precision of these estimates. As we will make clear below, the confidence one has in various CGE conclusions depends critically on the size of the confidence interval around parameter estimates. Standard “robustness checks” such as systematically raising or lowering the substitution parameters does not properly address this problem because it ignores information about which parameters we know with some precision and which we do not. A second problem with most existing studies derives from the use of import price series to identify home vs. foreign substitution, for example, tends to systematically understate the true elasticity. This is because these estimates take price variation as exogenous when estimating the import demand functions, and ignore quality variation. When quality is high, import demand and prices will be jointly high. This biases estimated elasticities toward zero. A related point is that the fixed-weight import price series used by most authors are theoretically inappropriate for estimating the elasticities of interest. CGE modelers generally examine a nested utility structure, with domestic production substitution for a CES composite import bundle. The appropriate price series is then the corresponding CES price index among foreign varieties. Constructing such an index requires knowledge of the elasticity of substitution among foreign varieties (see below). By using a fixed-weight import price series, previous estimates place too much weight on high foreign prices, and too small a weight on low foreign prices. In other words, they overstate the degree of price variation that exists, relative to a CES price index. Reconciling small trade volume movements with large import price series movements requires a small elasticity of substitution. This problem, and that of unmeasured quality variation, helps explain why typical estimated elasticities are very small. The third problem with the existing literature is that estimates taken from other researchers’ studies typically employ different levels of aggregation, and exploit different sources of price variation, from what policy modelers have in mind. Employment of elasticities in experiments ill-matched to their original estimation can be problematic. For example, estimates may be calculated at a higher or lower level of aggregation than the level of analysis than the modeler wants to examine. Estimating substitutability across sources for paddy rice gives one a quite different answer than estimates that look at agriculture as a whole. When analyzing Free Trade Agreements, the principle policy experiment is a change in relative prices among foreign suppliers caused by lowering tariffs within the FTA. Understanding the substitution this will induce across those suppliers is critical to gauging the FTA’s real effects. Using home v. foreign elasticities rather than elasticities of substitution among imports supplied from different countries may be quite misleading. Moreover, these “sourcing” elasticities are critical for constructing composite import price series to appropriate estimate home v. foreign substitutability. In summary, the history of estimating the substitution elasticities governing trade flows in CGE models has been checkered at best. Clearly there is a need for improved econometric estimation of these trade elasticities that is well-integrated into the CGE modeling framework. This paper provides such estimation and integration, and has several significant merits. First, we choose our experiment carefully. Our CGE analysis focuses on the prospective Free Trade Agreement of the Americas (FTAA) currently under negotiation. This is one of the most important FTAs currently “in play” in international negotiations. It also fits nicely with the source data used to estimate the trade elasticities, which is largely based on imports into North and South America. Our assessment is done in a perfectly competitive, comparative static setting in order to emphasize the role of the trade elasticities in determining the conventional gains/losses from such an FTA. This type of model is still widely used by government agencies for the evaluation of such agreements. Extensions to incorporate imperfect competition are straightforward, but involve the introduction of additional parameters (markups, extent of unexploited scale economies) as well as structural assumptions (entry/no-entry, nature of inter-firm rivalry) that introduce further uncertainty. Since our focus is on the effects of a PTA we estimate elasticities of substitution across multiple foreign supply sources. We do not use cross-exporter variation in prices or tariffs alone. Exporter price series exhibit a high degree of multicolinearity, and in any case, would be subject to unmeasured quality variation as described previously. Similarly, tariff variation by itself is typically unhelpful because by their very nature, Most Favored Nation (MFN) tariffs are non-discriminatory in nature, affecting all suppliers in the same way. Tariff preferences, where they exist, are often difficult to measure – sometimes being confounded by quantitative barriers, restrictive rules of origin, and other restrictions. Instead we employ a unique methodology and data set drawing on not only tariffs, but also bilateral transportation costs for goods traded internationally (Hummels, 1999). Transportation costs vary much more widely than do tariffs, allowing much more precise estimation of the trade elasticities that are central to CGE analysis of FTAs. We have highly disaggregated commodity trade flow data, and are therefore able to provide estimates that precisely match the commodity aggregation scheme employed in the subsequent CGE model. We follow the GTAP Version 5.0 aggregation scheme which includes 42 merchandise trade commodities covering food products, natural resources and manufactured goods. With the exception of two primary commodities that are not traded, we are able to estimate trade elasticities for all merchandise commodities that are significantly different form zero at the 95% confidence level. Rather than producing point estimates of the resulting welfare, export and employment effects, we report confidence intervals instead. These are based on repeated solution of the model, drawing from a distribution of trade elasticity estimates constructed based on the econometrically estimated standard errors. There is now a long history of CGE studies based on SSA: Systematic Sensitivity Analysis (Harrison and Vinod, 1992; Wigle, 1991; Pagon and Shannon, 1987) Ho

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