Un ejemplo de aportación de la didáctica de la física a la enseñanza : los ejercicios cualitativos y los razonamientos funcionales

Didactic specialists use exercises as a resource for research, whereas for teachers they are resources for teaching and evaluating. In most cases the evaluative exercises are of a quantitave type and the didactic value of the exercises of a qualitative type is not clearly shown. Starting frorn the analysis of the answers to exercises on the same subject but of different types, the author shows how important qiialitative exercises are and how they can be used as resources for teaching and evaluating

Atypical protein kinase C (PKCzeta/lambda) is a convergent downstream target of the insulin-stimulated phosphatidylinositol 3-kinase and TC10 signaling pathways.

Insulin stimulation of adipocytes resulted in the recruitment of atypical PKC (PKCzeta/lambda) to plasma membrane lipid raft microdomains. This redistribution of PKCzeta/lambda was prevented by Clostridium difficile toxin B and by cholesterol depletion, but was unaffected by inhibition of phosphatidylinositol (PI) 3-kinase activity. Expression of the constitutively active GTP-bound form of TC10 (TC10Q/75L), but not the inactive GDP-bound mutant (TC10/T31N), targeted PKCzeta/lambda to the plasma membrane through an indirect association with the Par6-Par3 protein complex. In parallel, insulin stimulation as well as TC10/Q75L resulted in the activation loop phosphorylation of PKCzeta. Although PI 3-kinase activation also resulted in PKCzeta/lambda phosphorylation, it was not recruited to the plasma membrane. Furthermore, insulin-induced GSK-3beta phosphorylation was mediated by both PI 3-kinase-PKB and the TC10-Par6-atypical PKC signaling pathways. Together, these data demonstrate that PKCzeta/lambda can serve as a convergent downstream target for both the PI 3-kinase and TC10 signaling pathways, but only the TC10 pathway induces a spatially restricted targeting to the plasma membrane

The Insulin receptor catalyzes the tyrosine phosphorylation o Caveolin 1

Our previous studies revealed that insulin stimulates the tyrosine phosphorylation of caveolin in 3T3L1 adipocytes. To explore the mechanisms involved in this event, we evaluated the association of the insulin receptor with caveolin. The receptor was detected in a Triton-insoluble low density fraction, co-sedimenting with caveolin and flotillin on sucrose density gradients. We also detected the receptor in caveolin-enriched rosette structures by immunohistochemical analysis of plasma membrane sheets from 3T3L1 adipocytes. Insulin stimulated the phosphorylation of caveolin-1 on Tyr14. This effect of the hormone was not blocked by overexpression of mutant forms of the Cbl-associated protein that block the translocation of phospho-Cbl to the caveolin-enriched, lipid raft microdomains. Moreover, this phosphorylation event was also unaffected by inhibitors of the MAPK and phosphatidylinositol 3-kinase pathways. Although previous studies demonstrated that the Src family kinase Fyn was highly enriched in caveolae, an inhibitor of this kinase had no effect on insulin-stimulated caveolin phosphorylation. Interestingly, overexpression of a mutant form of caveolin that failed to interact with the insulin receptor did not undergo phosphorylation. Taken together, these data indicate that the insulin receptor directly catalyzes the tyrosine phosphorylation of caveolin. Previous article in issu

Turning light into a liquid via atomic coherence

We study a four level atomic system with electromagnetically induced transparency with giant $\chi^{(3)}$ and $\chi^{(5)}$ susceptibilities of opposite signs. This system would allow to obtain multidimensional solitons and light condensates with surface tension properties analogous to those of usual liquids

Otopetrin 1 protects mice from obesity-associated metabolic dysfunction through attenuating adipose tissue inflammation.

Chronic low-grade inflammation is emerging as a pathogenic link between obesity and metabolic disease. Persistent immune activation in white adipose tissue (WAT) impairs insulin sensitivity and systemic metabolism, in part, through the actions of proinflammatory cytokines. Whether obesity engages an adaptive mechanism to counteract chronic inflammation in adipose tissues has not been elucidated. Here we identified otopetrin 1 (Otop1) as a component of a counterinflammatory pathway that is induced in WAT during obesity. Otop1 expression is markedly increased in obese mouse WAT and is stimulated by tumor necrosis factor-α in cultured adipocytes. Otop1 mutant mice respond to high-fat diet with pronounced insulin resistance and hepatic steatosis, accompanied by augmented adipose tissue inflammation. Otop1 attenuates interferon-γ (IFN-γ) signaling in adipocytes through selective downregulation of the transcription factor STAT1. Using a tagged vector, we found that Otop1 physically interacts with endogenous STAT1. Thus, Otop1 defines a unique target of cytokine signaling that attenuates obesity-induced adipose tissue inflammation and plays an adaptive role in maintaining metabolic homeostasis in obesity

Atypical Protein Kinase C (PKCλ/ζ) is a convergent downstream target of the insulin stimulated phosphatidylinositol 3-kinase and TC10 signalling pathways

Insulin stimulation of adipocytes resulted in the recruitment of atypical PKC (PKCζ/λ) to plasma membrane lipid raft microdomains. This redistribution of PKCζ/λ was prevented by Clostridium difficile toxin B and by cholesterol depletion, but was unaffected by inhibition of phosphatidylinositol (PI) 3-kinase activity. Expression of the constitutively active GTP-bound form of TC10 (TC10Q/75L), but not the inactive GDP-bound mutant (TC10/T31N), targeted PKCζ/λ to the plasma membrane through an indirect association with the Par6-Par3 protein complex. In parallel, insulin stimulation as well as TC10/Q75L resulted in the activation loop phosphorylation of PKCζ. Although PI 3-kinase activation also resulted in PKCζ/λ phosphorylation, it was not recruited to the plasma membrane. Furthermore, insulin-induced GSK-3β phosphorylation was mediated by both PI 3-kinase-PKB and the TC10-Par6-atypical PKC signaling pathways. Together, these data demonstrate that PKCζ/λ can serve as a convergent downstream target for both the PI 3-kinase and TC10 signaling pathways, but only the TC10 pathway induces a spatially restricted targeting to the plasma membrane

Collaboration Between Universities and Public Schools for Improved Student Achievement: A Report on the Progress of a Developing Partnership

This article reports the progress of one project aimed at bringing together professionals from post-secondary and K-12 environments. The project is being implemented at Richards Middle (RMS) in Columbus, Georgia and involves a collaborative partnership between several universities and RMS, resulting in a school-based evaluation initiative with direct implications for strengthening leadership, training, and instructional practices in schools. Faculty researchers from three universities from two states, Troy University, Columbus State University, and Auburn University are working collaboratively with faculty and staff of Richards Middle School on an inquiry with a three-fold purpose. The primary goal is to evaluate the effectiveness of the school’s International Baccalaureate (IB) Programme in its first year of implementation in the sixth grade. A second goal of the investigation is to evaluate the effectiveness of the staff training and development process employed during the initial year in terms of effective professional learning practices. A third goal is to investigate the effectiveness of the collaborative process itself in terms of the implementation of the dialogic approach discussed in Clark, et al. (1996)

Parametric localized modes in quadratic nonlinear photonic structures

We analyze two-color spatially localized modes formed by parametrically coupled fundamental and second-harmonic fields excited at quadratic (or chi-2) nonlinear interfaces embedded into a linear layered structure --- a quasi-one-dimensional quadratic nonlinear photonic crystal. For a periodic lattice of nonlinear interfaces, we derive an effective discrete model for the amplitudes of the fundamental and second-harmonic waves at the interfaces (the so-called discrete chi-2 equations), and find, numerically and analytically, the spatially localized solutions --- discrete gap solitons. For a single nonlinear interface in a linear superlattice, we study the properties of two-color localized modes, and describe both similarities and differences with quadratic solitons in homogeneous media.Comment: 9 pages, 8 figure

Lipid raft microdomain compartalization of TC10 is required for insulin signalling and Glut4 Translocation

Recent studies indicate that insulin stimulation of glucose transporter (GLUT)4 translocation requires at least two distinct insulin receptor-mediated signals: one leading to the activation of phosphatidylinositol 3 (PI-3) kinase and the other to the activation of the small GTP binding protein TC10. We now demonstrate that TC10 is processed through the secretory membrane trafficking system and localizes to caveolin-enriched lipid raft microdomains. Although insulin activated the wild-type TC10 protein and a TC10/H-Ras chimera that were targeted to lipid raft microdomains, it was unable to activate a TC10/K-Ras chimera that was directed to the nonlipid raft domains. Similarly, only the lipid raft-localized TC10/ H-Ras chimera inhibited GLUT4 translocation, whereas the TC10/K-Ras chimera showed no significant inhibitory activity. Furthermore, disruption of lipid raft microdomains by expression of a dominant-interfering caveolin 3 mutant (Cav3/DGV) inhibited the insulin stimulation of GLUT4 translocation and TC10 lipid raft localization and activation without affecting PI-3 kinase signaling. These data demonstrate that the insulin stimulation of GLUT4 translocation in adipocytes requires the spatial separation and distinct compartmentalization of the PI-3 kinase and TC10 signaling pathways