Dispositivos de formación profesional : Diálogos entre el campo de la investigación y de la formación profesional

En esta comunicación se intentan identificar algunas de las características específicas que pueden presentar los dispositivos de formación profesional de futuros docentes. A partir de los resultados de una investigación sobre la construcción de saberes pedagógicos en la acción desarrollada en el seno de un Grupo Profesional de Referencia en la que se recurre a autoconfrontaciones simples y cruzadas (Clot, 2004), se analizan los aportes teórico-metodológicos para la puesta en acción de dispositivos de formación profesional durante la formación inicial. La orientación teórico-metodológica adoptada pretende con la intención de construir saberes pedagógicos desde una perspectiva profesional contribuir a la generación de situaciones de formación. Dichas situaciones serían potencialmente capaces de hacer emerger, movilizar y poner en acción los saberes pedagógicos construidos por los formadores y por los estudiantes. Se propone entonces diseñar situaciones de formación que recuperen distintas culturas de acción pedagógica, construyendo nuevos sentidos en interacción con el medio profesional, el corpus disciplinar de la Pedagogía y la propia situación de formación. Finalmente se intenta avanzar sobre dos grupos de interrogantes a saber: La acción entendida como conjunto de actividades dotadas de una unidad de sentido y/o de significaciones en el ámbito de interacciones con otros sujetos (Barbier and Galatanu, 2000) se presentaría casi "invisible" a los ojos de los educadores en los dispositivos de formación más tradicionales ¿Cómo descubrir la acción en las situaciones de formación? Los dispositivos de formación profesional centrados en la emergencia de saberes pedagógicos en la acción trascienden la lógica secuencial de pensamiento y acción ¿Cómo poner en acción, cómo movilizar el saber pedagógico del formador en situaciones de formación? ¿Cuáles son los aportes que puede ofrecer el análisis de la actividad (Clot, 2004)? Es intención de esta ponencia proponer una serie de cuestiones que resitúen los aportes de la Pedagogía en el campo de la Formación contribuyendo a la formulación de nuevas preguntas que permitan orientar la acción.

An investigation of the performance of a new Mechanical thrombectomy device using Bond Graph modelling: application to the extraction of blood clots in the middle cerebral artery

A number of thrombectomy devices using a variety of methods have now been developed to facilitate clot removal. We present research involving one such experimental device recently developed in the UK, called a ‘GP’ Thrombus Aspiration Device (GPTAD). This device has the potential to bring about the extraction of a thrombus. Although the device is at a relatively early stage of development, the results look encouraging. In this work, we present an analysis and modeling of the GPTAD by means of the bond graph technique; it seems to be a highly effective method of simulating the device under a variety of conditions. Such modeling is useful in optimizing the GPTAD and predicting the result of clot extraction. The aim of this simulation model is to obtain the minimum pressure necessary to extract the clot and to verify that both the pressure and the time required to complete the clot extraction are realistic for use in clinical situations, and are consistent with any experimentally obtained data. We therefore consider aspects of rheology and mechanics in our modeling.

Applicability of the GP Device to the Circle of Willis Arteries by Using a Mathematical Model

According to the World Health Organization, 15 million people suffer stroke worldwide each year, of these, 5 million die and 5 million are permanently disabled. Stroke is therefore a major cause of mortality world-wide. The majority of strokes are caused by a blood clot that occludes an artery in the brain, and although thrombolytic agents such as Alteplase are used to dissolve clots that arise in the arteries of the brain, there are limitations on the use of these thrombolytic agents. However over the past decade, other methods of treatment have been developed which include Thrombectomy Devices e.g. the 'GP' Thrombus Aspiration Device ('GP' TAD). Such devices may be used as an alternative to thrombolytics or in conjunction with them to extract blood clots in arteries such as the middle cerebral artery of the midbrain brain, and the posterior inferior cerebellar artery (PICA) of the posterior aspect of the brain. In this paper, we mathematically model the removal of blood clots using the 'GP' TAD from selected arteries of the brain where blood clots may arise taking into account factors such as the resistances, compliances and inertances effects. Such mathematical modelling may have potential uses in predicting the pressures necessary to extract blood clots of given lengths, and masses from arteries in the Circle of Willis - posterior circulation of the brain

Analysis and design of a thrombectomy device by using simulation techniques

Purpose: In this work, we present the analysis, design and optimization of one experimental device recently developed in the UK, called the 'GP' Thrombus Aspiration Device (GPTAD). This device has been designed to remove blood clots without the need to make contact with the clot itself thereby potentially reducing the risk of problems such as downstream embolisation. Method: To obtain the minimum pressure necessary to extract the clot and to optimize the device, we have simulated the performance of the GPTAD analysing the resistances, compliances and inertances effects. We model a range of diameters for the GPTAD considering different forces of adhesion of the blood clot to the artery wall, and different lengths of blood clot. In each case we determine the optimum pressure required to extract the blood clot from the artery using the GPTAD, which is attached at its proximal end to a suction pump. Result: We then compare the results of our mathematical modelling to measurements made in laboratory using plastic tube models of arteries of comparable diameter. We use abattoir porcine blood clots that are extracted using the GPTAD. The suction pressures required for such clot extraction in the plastic tube models compare favourably with those predicted by the mathematical modelling. Discussion & Conclusion: We conclude therefore that the mathematical modelling is a useful technique in predicting the performance of the GPTAD and may potentially be used in optimising the design of the device.

Simulation of a mechanical thrombectomy device based in the use of self-expandable stents for the blood clots extraction

Recently, we have presented some studies concerning the analysis, design and optimization of one experimental device developed in the UK - GPTAD - which has been designed to remove blood clots without the need to make contact with the clot itself, thereby potentially reducing the risk of problems such as downstream embolisation. Based on the idea of a modification of the previous device, in this work, we present a model based in the use of stents like the SolitaireTM FR, which is in contact with the clot itself. In the case of such devices, the stent is self-expandable and the extraction of the blood clot is faciliatated by the stent, which must be inside the clot. Such stents are generally inserted in position by using the guidewire inserted into the catheter. This type of modeling could potentially be useful in showing how the blood clot is moved by the various different forces involved. The modelling has been undertaken by analyzing the resistances, compliances and inertances effects. We model an artery and blood clot for range of forces for the guidewire. In each case we determine the interaction between blood clot, stent and artery.

Prothrombin deficiency results in embryonic and neonatal lethality in mice

The conversion of prothrombin (FII) to the serine protease, thrombin (FIIa), is a key step in the coagulation cascade because FIIa triggers platelet activation, converts fibrinogen to fibrin, and activates regulatory pathways that both promote and ultimately suppress coagulation. However, several observations suggest that FII may serve a broader physiological role than simply stemming blood loss, including the identification of multiple G protein-coupled, thrombin-activated receptors, and the well-documented mitogenic activity of FIIa in in vitro test systems. To explore in greater detail the physiological roles of FII in vivo, FII-deficient (FII−/−) mice were generated. Inactivation of the FII gene leads to partial embryonic lethality with more than one-half of the FII−/− embryos dying between embryonic days 9.5 and 11.5. Bleeding into the yolk sac cavity and varying degrees of tissue necrosis were observed in many FII−/− embryos within this gestational time frame. However, at least one-quarter of the FII−/− mice survived to term, but ultimately they, too, developed fatal hemorrhagic events and died within a few days of birth. This study directly demonstrates that FII is important in maintaining vascular integrity during development as well as postnatal life.

Fibrinogen deficiency reduces vascular accumulation of apolipoprotein(a) and development of atherosclerosis in apolipoprotein(a) transgenic mice

To test directly whether fibrin(ogen) is a key binding site for apolipoprotein(a) [apo(a)] in vessel walls, apo(a) transgenic mice and fibrinogen knockout mice were crossed to generate fibrin(ogen)-deficient apo(a) transgenic mice and control mice. In the vessel wall of apo(a) transgenic mice, fibrin(ogen) deposition was found to be essentially colocalized with focal apo(a) deposition and fatty-streak type atherosclerotic lesions. Fibrinogen deficiency in apo(a) transgenic mice decreased the average accumulation of apo(a) in vessel walls by 78% and the average lesion (fatty streak type) development by 81%. Fibrinogen deficiency in wild-type mice did not significantly reduce lesion development. Our results suggest that fibrin(ogen) provides one of the major sites to which apo(a) binds to the vessel wall and participates in the generation of atherosclerosis.

Plasminogen deficiency accelerates vessel wall disease in mice predisposed to atherosclerosis

A critical link between hemostatic factors and atherosclerosis has been inferred from a variety of indirect observations, including the expression of procoagulant and fibrinolytic factors within atherosclerotic vessels, the presence of fibrin in intimal lesions, and the cellular infiltration of mural thrombi leading to their incorporation into developing plaques. To directly examine the role of the key fibrinolytic factor, plasminogen, in atherogenesis, plasminogen-deficient mice were crossed to hypercholesterolemic, apolipoprotein E-deficient mice predisposed to atherosclerosis. We report that the loss of plasminogen greatly accelerates the formation of intimal lesions in apolipoprotein E-deficient animals, whereas plasminogen deficiency alone does not cause appreciable atherosclerosis. These studies provide direct evidence that circulating hemostatic factors strongly influence vessel wall disease in the context of a disorder in lipid metabolism.

Convergent evolution of apolipoprotein(a) in primates and hedgehog

Apolipoprotein(a) [apo(a)] is the distinguishing protein component of lipoprotein(a), a major inherited risk factor for atherosclerosis. Human apo(a) is homologous to plasminogen. It contains from 15 to 50 repeated domains closely related to plasminogen kringle four, plus single kringle five-like and inactive protease-like domains. This expressed gene is confined to a subset of primates. Although most mammals lack apo(a), hedgehogs produce an apo(a)-like protein composed of highly repeated copies of a plasminogen kringle three-like domain, with complete absence of protease domain sequences. Both human and hedgehog apo(a)-like proteins form covalently linked lipoprotein particles that can bind to fibrin and other substrates shared with plasminogen. DNA sequence comparisons and phylogenetic analysis indicate that the human type of apo(a) evolved from a duplicated plasminogen gene during recent primate evolution. In contrast, the kringle three-based type of apo(a) evolved from an independent duplication of the plasminogen gene approximately 80 million years ago. In a type of convergent evolution, the plasminogen gene has been independently remodeled twice during mammalian evolution to produce similar forms of apo(a) in two widely divergent groups of species.

Plasminogen deficiency leads to impaired remodeling after a toxic injury to the liver

Cellular proliferation and tissue remodeling are central to the regenerative response after a toxic injury to the liver. To explore the role of plasminogen in hepatic tissue remodeling and regeneration, we used carbon tetrachloride to induce an acute liver injury in plasminogen-deficient (Plgo) mice and nontransgenic littermates (Plg+). On day 2 after CCl4, livers of Plg+ and Plgo mice had a similar diseased pale/lacy appearance, followed by restoration of normal appearance in Plg+ livers by day 7. In contrast, Plgo livers remained diseased for as long as 2.5 months, with a diffuse pale/lacy appearance and persistent damage to centrilobular hepatocytes. The persistent centrilobular lesions were not a consequence of impaired proliferative response in Plgo mice. Notably, fibrin deposition was a prominent feature in diseased centrilobular areas in Plgo livers for at least 30 days after injury. Nonetheless, the genetically superimposed loss of the Aα fibrinogen chain (Plgo/Fibo mice) did not correct the abnormal phenotype. These data show that plasminogen deficiency impedes the clearance of necrotic tissue from a diseased hepatic microenvironment and the subsequent reconstitution of normal liver architecture in a fashion that is unrelated to circulating fibrinogen.

Blood-borne tissue factor: Another view of thrombosis

Arterial thrombosis is considered to arise from the interaction of tissue factor (TF) in the vascular wall with platelets and coagulation factors in circulating blood. According to this paradigm, coagulation is initiated after a vessel is damaged and blood is exposed to vessel-wall TF. We have examined thrombus formation on pig arterial media (which contains no stainable TF) and on collagen-coated glass slides (which are devoid of TF) exposed to flowing native human blood. In both systems the thrombi that formed during a 5-min perfusion stained intensely for TF, much of which was not associated with cells. Antibodies against TF caused ≈70% reduction in the amount of thrombus formed on the pig arterial media and also reduced thrombi on the collagen-coated glass slides. TF deposited on the slides was active, as there was abundant fibrin in the thrombi. Factor VIIai, a potent inhibitor of TF, essentially abolished fibrin production and markedly reduced the mass of the thrombi. Immunoelectron microscopy revealed TF-positive membrane vesicles that we frequently observed in large clusters near the surface of platelets. TF, measured by factor Xa formation, was extracted from whole blood and plasma of healthy subjects. By using immunostaining, TF-containing neutrophils and monocytes were identified in peripheral blood; our data raise the possibility that leukocytes are the main source of blood TF. We suggest that blood-borne TF is inherently thrombogenic and may be involved in thrombus propagation at the site of vascular injury.

Muro Mediterráneo: búnkeres y baterías para la defensa del litoral (1936-1939)

The Mediterranean wall, which is a collection of defensive constructions along the coast, was built during the Spanish War (1936-39) to prevent enemy attacks. It´s called this way like the Atlantic Wall, which was built after the Second World War. These group of buildings consist of batteries, bunkers and barracks placed along the coastline, sometimes next to another kind of infrastructure. Its location (typical of a military strategy) and its peculiar morphology are like another ones: the historical watchtowers ones. They were built by the Kingdom of Spain in the same geography four centuries earlier although, in our case, the buildings are updated to the conditions of contemporary wars: camouflage against air raids. A collection of anti-aircraft devices, placed along the coast since the late 1937, were risen following the instructions of the Valencian State to defend both citizens and cities from the aviation´s bombings. The following military settlements, organized from North to South, are part of the most relevant ones of the coast of Alicante: the Denia and Javea ones, the North of Alicante and Southwest of Alicante ones, the Portichol one, the Galvany´s Clot one and, finally, the Cape and Bay of Santa Pola ones. Remains of more than 60 architectural elements, that document the first concrete´s ruins, are still there. This paper tries to document all of them (providing their location, their morphological genealogy and including some drawings of the current state) to contribute to their revaluation and to help to their necessary protection. They are a legacy of architectural heritage which consolidates and increases the memory of our culture.

Diagnosis and management of nonvariceal upper gastrointestinal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) Guideline

This Guideline is an official statement of the European Society of Gastrointestinal Endoscopy (ESGE). It addresses the diagnosis and management of nonvariceal upper gastrointestinal hemorrhage (NVUGIH). Main Recommendations MR1. ESGE recommends immediate assessment of hemodynamic status in patients who present with acute upper gastrointestinal hemorrhage (UGIH), with prompt intravascular volume replacement initially using crystalloid fluids if hemodynamic instability exists (strong recommendation, moderate quality evidence). MR2. ESGE recommends a restrictive red blood cell transfusion strategy that aims for a target hemoglobin between 7 g/dL and 9 g/dL. A higher target hemoglobin should be considered in patients with significant co-morbidity (e. g., ischemic cardiovascular disease) (strong recommendation, moderate quality evidence). MR3. ESGE recommends the use of the Glasgow-Blatchford Score (GBS) for pre-endoscopy risk stratification. Outpatients determined to be at very low risk, based upon a GBS score of 0 - 1, do not require early endoscopy nor hospital admission. Discharged patients should be informed of the risk of recurrent bleeding and be advised to maintain contact with the discharging hospital (strong recommendation, moderate quality evidence). MR4. ESGE recommends initiating high dose intravenous proton pump inhibitors (PPI), intravenous bolus followed by continuous infusion (80 mg then 8 mg/hour), in patients presenting with acute UGIH awaiting upper endoscopy. However, PPI infusion should not delay the performance of early endoscopy (strong recommendation, high quality evidence). MR5. ESGE does not recommend the routine use of nasogastric or orogastric aspiration/lavage in patients presenting with acute UGIH (strong recommendation, moderate quality evidence). MR6. ESGE recommends intravenous erythromycin (single dose, 250 mg given 30 - 120 minutes prior to upper gastrointestinal [GI] endoscopy) in patients with clinically severe or ongoing active UGIH. In selected patients, pre-endoscopic infusion of erythromycin significantly improves endoscopic visualization, reduces the need for second-look endoscopy, decreases the number of units of blood transfused, and reduces duration of hospital stay (strong recommendation, high quality evidence). MR7. Following hemodynamic resuscitation, ESGE recommends early (≤ 24 hours) upper GI endoscopy. Very early (< 12 hours) upper GI endoscopy may be considered in patients with high risk clinical features, namely: hemodynamic instability (tachycardia, hypotension) that persists despite ongoing attempts at volume resuscitation; in-hospital bloody emesis/nasogastric aspirate; or contraindication to the interruption of anticoagulation (strong recommendation, moderate quality evidence). MR8. ESGE recommends that peptic ulcers with spurting or oozing bleeding (Forrest classification Ia and Ib, respectively) or with a nonbleeding visible vessel (Forrest classification IIa) receive endoscopic hemostasis because these lesions are at high risk for persistent bleeding or rebleeding (strong recommendation, high quality evidence). MR9. ESGE recommends that peptic ulcers with an adherent clot (Forrest classification IIb) be considered for endoscopic clot removal. Once the clot is removed, any identified underlying active bleeding (Forrest classification Ia or Ib) or nonbleeding visible vessel (Forrest classification IIa) should receive endoscopic hemostasis (weak recommendation, moderate quality evidence). MR10. In patients with peptic ulcers having a flat pigmented spot (Forrest classification IIc) or clean base (Forrest classification III), ESGE does not recommend endoscopic hemostasis as these stigmata present a low risk of recurrent bleeding. In selected clinical settings, these patients may be discharged to home on standard PPI therapy, e. g., oral PPI once-daily (strong recommendation, moderate quality evidence). MR11. ESGE recommends that epinephrine injection therapy not be used as endoscopic monotherapy. If used, it should be combined with a second endoscopic hemostasis modality (strong recommendation, high quality evidence). MR12. ESGE recommends PPI therapy for patients who receive endoscopic hemostasis and for patients with adherent clot not receiving endoscopic hemostasis. PPI therapy should be high dose and administered as an intravenous bolus followed by continuous infusion (80 mg then 8 mg/hour) for 72 hours post endoscopy (strong recommendation, high quality evidence). MR13. ESGE does not recommend routine second-look endoscopy as part of the management of nonvariceal upper gastrointestinal hemorrhage (NVUGIH). However, in patients with clinical evidence of rebleeding following successful initial endoscopic hemostasis, ESGE recommends repeat upper endoscopy with hemostasis if indicated. In the case of failure of this second attempt at hemostasis, transcatheter angiographic embolization (TAE) or surgery should be considered (strong recommendation, high quality evidence). MR14. In patients with NVUGIH secondary to peptic ulcer, ESGE recommends investigating for the presence of Helicobacter pylori in the acute setting with initiation of appropriate antibiotic therapy when H. pylori is detected. Re-testing for H. pylori should be performed in those patients with a negative test in the acute setting. Documentation of successful H. pylori eradication is recommended (strong recommendation, high quality evidence). MR15. In patients receiving low dose aspirin for secondary cardiovascular prophylaxis who develop peptic ulcer bleeding, ESGE recommends aspirin be resumed immediately following index endoscopy if the risk of rebleeding is low (e. g., FIIc, FIII). In patients with high risk peptic ulcer (FIa, FIb, FIIa, FIIb), early reintroduction of aspirin by day 3 after index endoscopy is recommended, provided that adequate hemostasis has been established (strong recommendation, moderate quality evidence).

Vindicias de la Sagrada Biblia contra los tiros de la incredulidad y su defensa y justificación de toda nota de contrariedad con la humana razon ... /

Contiene: T. I (XIV, 444 p.) -- T. II (392 p.) -- T. III (412 p.) -- T. IV (508 p.) -- T. V (510 p.) -- T. VI (384 p.) -- T. VII (376 p.)

De la peste observée en Égypte : recherches et considérations sur cette maladie /

Mode of access: Internet.