| 18271. |
- Zlatev, Jordan
(författare)
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From proto-mimesis to language: Evidence from primatology and social neuroscience.
- 2008
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Ingår i: Journal of Physiology - Paris. - : Elsevier BV. - 1769-7115 .- 0928-4257. ; 102:1-3, s. 137-151
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Tidskriftsartikel (refereegranskat)abstract
- How can we reconcile the conception of language as a conventional-normative semiotic system with a perception/action-based account of its structure and meaning? And why should linguistic meaning - as opposed to linguistic expression - be so closely related to motor activity and its neural underpinnings, as suggested by recent findings? A conceptual framework and evolutionary scenario building on the concept of bodily mimesis [Zlatev, J., 2005. What's in a schema? Bodily mimesis and the grounding of language. In: Hampe, B. (Ed.), From Perception to Meaning: Image Schemas in Cognitive Linguistics. Mouton de Gruyter, Berlin, pp. 313-343] imply answers to these questions. The article presents evidence for a particular evolutionary stage model by reviewing recent evidence on the capacity of non-human primates for intersubjectivity, imitation and gestural communication, and from neuroscientific studies of these capacities in monkeys and human subjects. It is argued that "mirror neuron" systems can subserve basic motoric and social capacities, but they need to be considerably extended in order to provide an efficient basis for bodily mimesis, and even more so for language. It is argued that while language may be ultimately "grounded" in perception and action, it is essential not to try to reduce it to them.
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| 18272. |
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| 18273. |
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| 18274. |
- Zlatev, Jordan
(författare)
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The dependence of language on consciousness
- 2008
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Ingår i: Journal of Consciousness Studies. - 1355-8250. ; 15:6, s. 34-62
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Tidskriftsartikel (refereegranskat)abstract
- For we have the experience of ourselves, of that consciousness which we are, and it is on the basis of this experience that all linguistic connotations are assessed, and precisely through it that language comes to have any meaning at all for us.
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| 18275. |
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| 18276. |
- Zlatev, Jordan
(författare)
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The semiotic hierarchy: life, consciousness, signs and language
- 2009
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Ingår i: Cognitive Semiotics. - 2235-2066. ; 4, s. 169-200
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Tidskriftsartikel (refereegranskat)abstract
- This article outlines a general theory of meaning, The Semiotic Hierarchy, which distinguishes between four major levels in the organization of meaning: life, consciousness, sign function and language, where each of these, in this order, both rests on the previous level, and makes possible the attainment of the next. This is shown to be one possible instantiation of the Cognitive Semiotics program, with influences from phenomenology, Popper’s tripartite ontology, semiotics, linguistics, enactive cognitive science and evolutionary biology. Key concepts such as “language” and “sign” are defined, as well as the four levels of The Semiotic Hierarchy, on the basis of the type of (a) subject, (b) value-system and (c) world in which the subject is embedded. Finally, it is suggested how the levels can be united in an evolutionary framework, assuming a strong form of emergence giving rise to “ontologically” new properties: consciousness, signs and languages, on the basis of a semiotic, though not standardly biosemiotic, understanding of life.
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| 18277. |
- Zlatev, Jordan, et al.
(författare)
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Triadic bodily mimesis is the difference
- 2005
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Ingår i: Behavioral and Brain Sciences. - 1469-1825. ; 28:5, s. 720-720
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- We find that the nature and origin of the proposed "dialogical cognitive representations" in the target article is not sufficiently clear. Our proposal is that (triadic) bodily mimesis and in particular mimetic schemas-prelinguistic representational, intersubjective structures, emerging through imitation but subsequently interiorized-can provide the necessary link between private sensory-motor experience and public language. In particular, we argue that shared intentionality requires triadic mimesis.
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| 18278. |
- Zlotta, AR, et al.
(författare)
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Hormone therapy: Improving therapy decisions and monitoring
- 2006
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Ingår i: European Urology. Supplement. - : Elsevier BV. - 1569-9056. ; 5:3, s. 369-376
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: Due to the increased diagnosis of prostate cancer at earlier stages and the overall increased use of hormone therapy, also in earlier disease stages, many patients will receive long-term hormone therapy. Therefore, the timing of initiating hormone therapy and the type of hormone therapy have become crucial items in the appropriate management of patients with prostate cancer. in addition, as patients receiving long-term hormone therapy are at an increased risk of acute and chronic side effects, the monitoring of these patients deserves attention. The timing and type of hormone therapy and the monitoring of patients receiving hormone therapy are reviewed in this paper. Methods: A literature review was performed in Medline. Results: The prostate specific antigen doubling time (PSA DT) has been evaluated to determine the risk of disease progression in patients having a relapse after radical therapy. Patients with a PSA DT of < 12 mo have a high risk for disease progression and should probably receive hormone therapy rapidly. In case of a diagnosis of advanced prostate cancer, there is not yet a consensus on when to start hormone therapy. During an interactive voting session, over 200 urologists indicated that the preferred luteinizing hormone releasing hormone (LHRH) agonist should be able to achieve a castrate level of <= 20 ng/dl, as well as to maintain these low testosterone levels without inducing acute-on-chronic or breakthrough responses. Eligard, a novel depot formulation of leuprolide acetate, appears to be the only LHRH agonist currently available able to achieve and maintain serum testosterone levels below the castrate level of 20 ng/dl. Patients receiving long-term hormone therapy should be adequately monitored during follow-up visits. Besides frequent assessment of the PSA level and other recommended assessments, serum testosterone levels should also be determined. In this way, response to therapy can be evaluated, relevant testosterone rises after initial treatment response can be detected, and potential reasons for unexpected PSA rises can be verified, which will improve the monitoring of patients receiving hormone therapy. Conclusions: Measuring testosterone levels before and during therapy initiation might improve hormone therapy decisions and monitoring. Eligard is an interesting LHRH agonist because it is able to achieve and maintain testosterone levels below 20 ng/dl. (c) 2006 Elsevier B.V. All rights reserved.
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| 18279. |
- Zmuda-Trzebiatowska, Emilia, et al.
(författare)
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Novel mechanisms of the regulation of Protein kinase B in adipocytes; implications for Protein kinase A, Epac, Phosphodiesterases 3 and 4.
- 2007
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Ingår i: Cellular Signalling. - : Elsevier BV. - 1873-3913 .- 0898-6568. ; 19:1, s. 81-86
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Tidskriftsartikel (refereegranskat)abstract
- Crosstalk between insulin and cAMP signalling pathways has a great impact on adipocyte metabolism. Whilst Protein kinase B (PKB) is a pivotal mediator of insulin action, in some cells regulation of PKB by cAMP has also been demonstrated. Here we provide evidence that, in a phosphatidyl inositol 3-kinase dependent manner, beta 3-adrenergic stimulation (using CL316243) in adipocytes induces PKB phosphorylation in the absence of insulin and also potentiates insulin-induced phosphorylation of PKB. Interestingly, insulin- and CL316243-induced PKB phosphorylation was found to be inhibited by pools of cAMP controlled by PDE3B and PDE4 (mainly in the context of insulin), whereas a cAMP pool controlling protein kinase A appeared to mediate stimulation of PKB phosphorylation (mainly in the context of CL316243). Furthermore, an Epac (exchange protein directly activated by cAMP) agonist (8-pCPT-2'-O-Me-cAMP) mimicked the effect of the PDE inhibitors, giving evidence that Epac has an inhibitory effect on PKB phosphorylation in adipocytes. Further, we put the results obtained at the level of PKB in the context of possible downstream signalling components in the regulation of adipocyte metabolism. Thus, we found that overexpression of PKB induced lipogenesis in a PDE3B-dependent manner. Furthermore, overexpression or inhibition of PDE3B was associated with reduced or increased phosphorylation of the key lipogenic enzyme acetyl-CoA carboxylase (ACC), respectively. These PDE3B-dependent effects on ACC correlated with changes in lipogenesis. The Epac agonist, 8-pCPT-2'-O-Me-cAMP, mimicked the effect of PDE3B inhibition on ACC phosphorylation and lipogenesis. (c) 2006 Elsevier Inc. All rights reserved.
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| 18280. |
- Zmuda-Trzebiatowska, Emilia, et al.
(författare)
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Role of PDE3B in insulin-induced glucose uptake, GLUT-4 translocation and lipogenesis in primary rat adipocytes.
- 2006
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Ingår i: Cellular Signalling. - : Elsevier BV. - 1873-3913 .- 0898-6568. ; 18:3, s. 382-390
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Tidskriftsartikel (refereegranskat)abstract
- In adipocytes, phosphorylation and activation of PDE3B is a key event in the antilipolytic action of insulin. The role of PDE4, another PDE present in adipocytes, is not yet known. In this work we investigate the role of PDE3B and PDE4 in insulin-induced glucose uptake, GLUT-4 translocation and lipogenesis. Inhibition of PDE3 (OPC3911, milrinone) but not PDE4 (RO 20-1724) lowered insulin-induced glucose uptake and lipogenesis, especially in the presence of isoproterenol (a general beta-adrenergic agonist), CL316243, a selective beta 3-adrenergic agonist, and pituitary adenylate cyclase-activating peptide. The inhibitory effect of OPC3911 was associated with reduced translocation of GLUT-4 from the cytosol to the plasma membrane. Both OPC3911 and RO 20-1724 increased protein kinase A (PKA) activity and lipolysis. H89, a PKA inhibitor, did not affect OPC3911-mediated inhibition of insulin-induced glucose uptake and lipogenesis, whereas 8-pCPT-2'-O-Me-cAMP, an Epac agonist which mediates PKA independent cAMP signaling events, mimicked all the effects of OPC3911. Insulin-mediated activation of protein kinase B, a kinase involved in insulin-induced glucose uptake, was apparently not altered by OPC3911. In summary, our data suggest that PDE3B, but not PDE4, contributes to the regulation of insulin-induced glucose uptake, GLUT-4 translocation, and lipogenesis presumably by regulation of a cAMP/Epac signalling mechanisms. (c) 2005 Elsevier Inc. All rights reserved.
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