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En este artículo se describen las prótesis usadas en las personas adultas que han sufrido una amputación del miembro inferior, por causa vascular (la gran mayoría), traumática, neoplásica, infecciosa o congénita, pero sin incluir las prótesis que no se ajustan a las «normas» y que se pueden encontrar en esta última causa. Expresa el punto de vista del ortoprotésico y del rehabilitador. En la primera parte, se describen las distintas prótesis que se utilizan en la actualidad. Después, se detalla su colocación, enumerando distintas técnicas y ofreciendo los consejos del rehabilitador sobre algunos diseños. Como conclusión, los autores presentan de un modo crítico, pero constructivo, algunos de los sistemas protésicos más avanzados.

Questo articolo presenta l’apparecchiatura per le persone adulte amputate agli arti inferiori, per causa vascolare (la maggior parte), traumatica, neoplastica, infettiva o congenita, ma senza mostrare le apparecchiature “non standard” che si possono trovare in quest’ultimo caso. Questo articolo esprime il punto di vista del costruttore e il punto di vista del rieducatore. Prima di tutto, sono esposte le varie protesi che vengono attualmente realizzate, con il supporto finanziario. Poi, viene spiegata in dettaglio l’applicazione dei dispositivi elencando varie tecniche e dando l’opinione del rieducatore su certi concetti. In conclusione, gli autori presentano, in modo critico ma costruttivo, alcuni sistemi protesici avanzati.

L’objectif de l’étude a été de tester l’efficacité d’une nouvelle orthèse limitant simultanément la mobilité de la cheville et du médio-pied dans les entorses de gravité modérée (grade I) à moyenne (grade II). L’étude était randomisée, multicentrique, conduite en ouvert, le choix de l’orthèse se faisant par tirage au sort. Le suivi de chaque patient s’est fait sur une période de 4 semaines. La durée totale de l’étude a été de 14 mois. Quatre vingt un dossiers de données ont pu être analysés statistiquement.

This paper sets out an identification method for the thermal conductivity λand the heat capacity per unit volume ρcof a polymer material. The measurement of the temperature is registered with infrared camera. An inverse reading of the F.E.M. allows to perform this identification by solving a linear algebraic system coming from a least square method. The relative uncertainty obtained in experimental case are very good.

A Stark pattern with hyperfine structure of CD3Cl, in thev2 andv5 bands region, was recorded with the 9P38 CO2 laser line. Besides the conventional one-photon transitions due tov2 andv5 lines, three two-photon resonance transitions, without Doppler broadening, were observed. They were assigned to the PQ(6,6) and PQ(7,6) of thev2+v5 band.

Les protéines G hétérotrimériques sont les intermédiaires clés permettant de transmettre les signaux extracellulaires reçus par les récepteurs couplés aux protéines G (RCPG) aux effecteurs. Ces protéines sont composées de trois sous-unités : la sous-unité Gα et les sous-unités Gβ et Gγ formant le dimère Gβγ. Le repliement de la sous-unité Gβ est facilité par le complexe cytosolique de la chaperonine (CCT) et par la protéine PhLP-1. Nous avons récemment décelé une protéine jouant le rôle de chaperonne moléculaire pour la sous-unité Gγ : la protéine de 78 kDa interagissant avec le récepteur à la dopamine (DRiP78), qui est une protéine résidente du réticulum endoplasmique. Nous avons observé une interaction entre les protéines PhLP-1 et DRiP78, ce qui suggère que ces deux chaperonnes, en plus de jouer un rôle dans les repliements des sousunités Gβ et Gγ, prendraient une importante part dans l’assemblage des sous-unités Gβ et Gγ en un dimère, processus encore mal compris. Cependant, beaucoup reste à faire avant de bien comprendre les mécanismes en jeu dans l’assemblage des hétérotrimères spécifiques. En effet, aucune chaperonne moléculaire n’a encore été détectée pour la sous-unité Gα et les mécanismes de l’interaction de la sous-unité Gα naissante et du dimère Gβγ nouvellement assemblé ne sont pas encore connus.

The physiological function of angiotensin II (Ang II) is mediated through the Ang II type 1 (AT1R) and type 2 (AT2R) receptors. Our previous studies have demonstrated that cell surface targeting of AT1R is regulated by Rab and Sar1 GTPases and the F(x)6LL motif in the membrane-proximal C terminus. However, the molecular mechanisms underlying the export of nascent AT2R remain poorly defined. In this report, we determined the role of Rab1 GTPase, which specifically controls protein transport from the endoplasmic reticulum (ER) to the Golgi, and receptor dimerization in the biosynthesis of AT2R. Cell surface expression of AT2R was augmented by transient expression of Rab1 and attenuated by dominant-negative Rab1 mutants and small interfering RNA-mediated knockdown of Rab1. Consistently, AT2R inhibition of epidermal growth factor-activated extracellular signal-regulated kinase 1/2 was significantly reduced by the Rab1 mutants, indicating that endogenous Rab1 modulates the cell surface targeting and signaling of AT2R. It is of interest to note that Rab1 augmented the overall expression of AT2R and its mRNA, whereas the Rab1 mutants attenuated the total AT2R expression and enhanced ubiquitin-dependent AT2R degradation. Furthermore, our previously characterized ER export-deficient AT1R mutant in which the F(x)6LL motif was mutated formed both homodimers and heterodimers with AT2R. Dimerization of the AT1R mutant with AT2R blocked AT2R trafficking to the cell surface, suggesting constitutive dimerization of both receptors in the ER and an important role of dimerization in ER export of the receptors. These data demonstrate for the first time that Rab1 GTPase and dimerization modulate export traffic from the ER to the cell surface of newly synthesized AT2R.

The physiological function of angiotensin II (Ang II) is mediated through the Ang II type 1 (AT1R) and type 2 (AT2R) receptors. Our previous studies have demonstrated that cell surface targeting of AT1R is regulated by Rab and Sar1 GTPases and the F(x)(6)LL motif in the membrane-proximal C terminus. However, the molecular mechanisms underlying the export of nascent AT2R remain poorly defined. In this report, we determined the role of Rab1 GTPase, which specifically controls protein transport from the endoplasmic reticulum (ER) to the Golgi, and receptor dimerization in the biosynthesis of AT2R. Cell surface expression of AT2R was augmented by transient expression of Rab1 and attenuated by dominant-negative Rab1 mutants and small interfering RNA-mediated knockdown of Rab1. Consistently, AT2R inhibition of epidermal growth factor-activated extracellular signal-regulated kinase 1/2 was significantly reduced by the Rab1 mutants, indicating that endogenous Rab1 modulates the cell surface targeting and signaling of AT2R. It is of interest to note that Rab1 augmented the overall expression of AT2R and its mRNA, whereas the Rab1 mutants attenuated the total AT2R expression and enhanced ubiquitin-dependent AT2R degradation. Furthermore, our previously characterized ER export-deficient AT1R mutant in which the F(x)(6)LL motif was mutated formed both homodimers and heterodimers with AT2R. Dimerization of the AT1R mutant with AT2R blocked AT2R trafficking to the cell surface, suggesting constitutive dimerization of both receptors in the ER and an important role of dimerization in ER export of the receptors. These data demonstrate for the first time that Rab1 GTPase and dimerization modulate export traffic from the ER to the cell surface of newly synthesized AT2R.

Insulin resistance in patients with latent autoimmune diabetes of adulthood (LADA) was determined by homeostasis model assessment (HOMA). LADA was identified by a clinical phenotype of type 2 diabetes with antibodies to GAD65 andor IA-2ICA512. All patients were managed with insulin therapy. Insulin resistance in LADA was lower than in antibody-negative type 2 diabetes, higher than in normal humans and in recent-onset type 1 diabetes, and similar to that in long-term type 1 diabetes. Mean values for HOMA varied linearly with mean values for BMI, which accounted for much of the insulin resistance in these forms of diabetes. LADA resembles long-term type 1 diabetes with respect to insulin resistance and BMI, but occurs at an older age.

We examined the frequencies of autoantibodies to glutamate decarboxylase, GAD65, protein tyrosine phosphatase, IA-2ICA512, and insulin, and of HLA class II markers in ICA-positive first-degree relatives of patients with type 1 diabetes. Our results indicate that while the presence of HLA susceptibility markers is associated with anti-islet autoantibodies, protective DQB1 markers do not absolutely prevent development of autoantibodies or progression to autoimmune diabetes.

As with most G-protein-coupled receptors, repeated agonist stimulation of the platelet-activating factor receptor (PAFR) results in its desensitization, sequestration, and internalization. In this report, we show that agonist-induced PAFR internalization is independent of G-protein activation but is dependent on arrestins and involves the interaction of arrestins with a limited region of the PAFR C terminus. In cotransfected COS-7 cells, both arrestin-2 and arrestin-3 could be coimmunoprecipitated with PAFR, and agonist stimulation of PAFR induced the translocation of both arrestin-2 and arrestin-3. Furthermore, coexpression of arrestin-2 with PAFR potentiated receptor internalization, whereas agonist-induced PAFR internalization was inhibited by a dominant negative mutant of arrestin-2. The coexpression of a minigene encoding the C-terminal segment of the receptor abolished PAF-induced arrestin translocation and inhibited PAFR internalization. Using C terminus deletion mutants, we determined that the association of arrestin-2 with the receptor was dependent on the region between threonine 305 and valine 330 because arrestin-2 could be immunoprecipitated with the mutant PAFRstop330 but not PAFRstop305. Consistently, stop330 could mediate agonist-induced arrestin-2 translocation, whereas stop305 could not. Two other deletion mutants with slightly longer regions of the C terminus, PAFRstop311 and PAFRstop317, also failed to induce arrestin-2 translocation. Finally, the PAFR mutant Y293A, containing a single substitution in the putative internalization motif DPXXY in the seventh transmembrane domain (which we had shown to be able to internalize but not to couple to G-proteins) could efficiently induce arrestin translocation. Taken together, our results indicate that ligand-induced PAFR internalization is dependent on arrestins, that PAFR can associate with both arrestin-2 and -3, and that their translocation involves interaction with the region of residues 318–330 in the PAFR C terminus but is independent of G-protein activation.

The receptor for platelet-activating factor (PAFR) is a member of the G protein-coupled receptor (GPCR) family. According to the allosteric ternary complex model, GPCRs exist in an equilibrium between different conformations. Agonist binding promotes and stabilizes the receptor in an active conformation. On the other hand, ligands that stabilize the inactive conformation are known as inverse agonists. Due to the association of platelet-activating factor (PAF) with diverse physiological and pathological processes, considerable efforts have been invested in the development of antagonists to PAFR. A large number of these molecules has been shown to specifically interact with PAFR but, surprisingly, little is known about their impact on the conformation of the receptor and its activity. By using a constitutively active mutant (L231R) of the human PAFR and by transiently coexpressing the wild-type (WT) receptor with the Gαqsubunit of the trimeric G protein, we were able to address this issue with ligands of diverse structures such as phospholipids, benzodiazepines, furans, and others. We demonstrated that some of these molecules are potent inverse agonists. For example, when cells (WT PAFR + Gαq) were exposed to WEB2086, SM10661, or alprazolam, the basal inositol phosphate production was reduced by 53 ± 6, 44 ± 3, and 54 ± 4%, respectively. The decrease in basal inositol phosphate production by WEB2086 was significantly inhibited by a more neutral antagonist BN52021, confirming the specificity of the reaction. We demonstrate here that WEB2086 and other known ligands previously considered as antagonists can act as inverse agonists on the human PAF receptor.

The υ5 band of methylacetylene has been studied simultaneously by means of CO2 Laser Stark spectroscopy and high resolution infrared absorption spectroscopy (0.012 cm−1). The primary aim of this work was to assign all the Stark coïncidences. Effective vibration-rotation parameters and the dipole moment of the v5=1 state have been determined.

The authors show a nondestructive method for obtaining the isochromatic and isoclinic fringes in a three-dimensional photoelastic specimen. The basic idea is to delimit a slice between two plane laser beams. The properties of polarization of the scattered light (Rayleigh's law) and the interference possibilities of the diffused beams are used. By introducing speckle pattern properties, the correlation factor of the two scattered beams is similar to the illumination given in a plane polariscope for the investigation of a slice (in a classical frozen-stress technique). The authors use a monochromatic laser beam, a CCD camera and a personal computer. Because they cannot obtain the correlation factor directly, they do a statistical analysis of the speckle patterns. The variance (function of the correlation factor) is computed from the light intensities of three images corresponding to the speckle pattern for plane 1 alone, plane 2 alone, and both planes together.

In the Canadian/European randomized controlled study on cyclosporin A (CsA) in recent onset Type 1 (insulin-dependent) diabetes, treatment with the immunosuppressive drug had increased and maintained Beta-cell function and clinical remission during the first 12 months. Following discontinuation of the study drug and double-blinding after a mean of 13.8 months former CsA patients doubled the daily insulin dose within 6 months reaching the level of former placebo patients. The difference in Beta-cell function between the two groups was also lost. Metabolic control (HbA1c) was transiently worse in the former CsA group. Adverse effects of cyclosporin A on systolic blood pressure, haemoglobin levels, serum potassium and creatinine levels also remitted during that time. We conclude that treatment with cyclosporin A for a mean of 13.8 months had no long-lasting effect on the course of Type 1 diabetes persisting beyond drug discontinuation.

Abstract: Recent results have suggested thatp,tert.-octylphenoxynonaethoxyethanol (OPE10) has a high degree of degradability. These results have been confirmed and extended. The loss of response to cobalt thiocyanate under a wide variety of laboratory test conditions demonstrates that OPE10 will readily undergo bacterial attack. Significant loss of foaming and ethylene oxide in laboratory continuous and semicontinuous activated sludge units and septic tank-percolation field units demonstrate that the degree of degradation under reasonable conditions can be extensive. Tracer studies and oxygen consumption tests are used to support this conclusion. These results indicate that OPE10 should be adequately degraded in conventional sewage disposal systems.