The poverty of economism: freedom, calculation, and the law

Karl Popper y Friedrich von Hayek son recordados como dos de los mayores defensores en el siglo XX, del  concepto de sociedad abierta. Ambos nacieron en Viena. Ambos se sintieron atraídos hacia el socialismo en  sus años mozos, y los dos escribieron críticas seminales contra el socialismo, que revelaban sus defectos  fundamentales. También eran muy buenos amigos, que se ayudaron mutuamente en sus carreras, y  generalmente se los consideró aliados filosóficos. Sin embargo, los puntos de vista de Hayek sobre la  democracia, la racionalidad y el economicismo, eran fundamentalmente opuestos a los de Popper -e incluso  quizás- a la sociedad abierta en sí.  El presente artículo, se centra en sus diferencias sobre el economicismo.Argumenta que la crítica popperiana al economicismo de Marx, también puede aplicarse a Hayek; que éste estaba “preparado” para aceptar el socialismo si pudiera ser tan eficiente y productivo como el mercado; que Popper no; y que es imposible realizar la idea de Hayek sobre la libertad por la misma razón que éste pensaba que el socialismo no podría tener éxito.Karl Popper and Friedrich von Hayek are remembered as two of the 20th century’s greatest proponents of  open society. They both were born in Vienna. They both were attracted to socialism early in life. And they  both wrote seminal critiques of socialism that revealed its fundamental flaws. They were also very close  friends, helped each other in their careers, and were generally regarded as philosophical allies. But Hayek’s  views about democracy, rationality, and economism are fundamentally at odds with Popper’s -and perhaps  even- with open society itself. This paper focuses upon their differences about economism. It argues that  Popper’s critique of Marx’s economism also applies to Hayek; that Hayek was ‘prepared’ to accept socialism  if it could be as efficient and productive as the market; that Popper wasn’t; and that it is impossible to realize  Hayek’s idea of freedom for the very same reason that Hayek thought socialism could not succeed

Verdad, racionalidad y situación

El principio de racionalidad afirma que las personas actúan de manera adecuada según su situación, pero no  especifica cómo deben actuar para hacerlo. El análisis situacional utiliza el principio de racionalidad, junto  con un modelo de situación social, para explicar las acciones en el pasado. A diferencia de la Teoría de la  Elección Racional, el análisis situacional no trata de predecir o influir en las acciones en el futuro. Popper  consideraba al principio de racionalidad como falso, pero, no obstante, pensaba que debíamos usarlo. Esto  plantea un problema para entender su punto de vista acerca de las conjeturas y refutaciones. Popper, sin  embargo, pensaban que todos los modelos científicos son falsos, así que si debemos o no rechazar un  modelo científico depende del problema que estamos tratando de resolver.The Rationality Principle says that people act adequately to their situation, but does not specify how they must  act in order to do so. Situational Analysis uses the Rationality Principle, together with a model of the social  situation, to explain actions in the past. Unlike Rational Choice Theory, Situational Analysis does not try to  predict or influence actions in the future. Popper regarded the Rationality Principle as false, but thought that we should use it nonetheless. This poses a problem for understanding his views about conjectures and refutations.  Popper, however, thought that all scientific models are false, and that whether or not we should reject a model  depends on the problem that we are trying to solve

Community Study, Wilmington Metropolitan Area

The purpose of this Community Study is to provide essential information for the pastors and lay leaders of the Seventh-day Adventist churches in the Wilmington metropolitan area and the steering committee of the Wilmington Area Adventist Community Services Agency. It is designed to assess community needs, potential partnerships, and opportunities for humanitarian ministry, as well as provide basic information about demographics.https://digitalcommons.andrews.edu/hrsa/1004/thumbnail.jp

Neuropathophysiological potential of Guillain-Barré syndrome anti-ganglioside-complex antibodies at mouse motor nerve terminals

Objectives:  Anti-ganglioside antibodies are present in approximately half of Guillain–Barré syndrome (GBS) patients. Recently, it has been shown that a considerable proportion of these patients has serum antibodies against antigenic epitopes formed by a complex of two different gangliosides. However, direct experimental evidence for neuropathogenicity of this special category of antibodies is currently lacking. Here, we explored a series of GBS and GBS-variant sera with anti-ganglioside-complex antibodies for their ability to induce complement-dependent deleterious effects at the living neuronal membrane. Methods:  The neuropathophysiological potential of 31 GBS sera containing either anti-GM1/GD1a- or anti-GM1/GQ1b-ganglioside-complex antibodies was studied at motor nerve terminal presynaptic membranes in the mouse phrenic nerve/diaphragm muscle ex vivo experimental model. With electrophysiological measurements and confocal fluorescence microscopy, we assessed and quantified the damaging effect on neuronal membranes by anti-ganglioside-complex antibodies. Results:  We show that anti-GM1/GD1a- and anti-GM1/GQ1b-ganglioside-complex positive sera can induce complement-mediated functional and morphological injury at mouse motor nerve terminals ex vivo. Of the 31 investigated anti-ganglioside-complex patient sera, 17 sera induced increases in miniature end-plate potential frequency in this experimental model, mostly associated with muscle fibre twitches. Variability in potency was observed, with the anti-GM1/GD1a-complex sera inducing the most outspoken effects.<b></b> Conclusions:  The present study shows the presence of ganglioside-complexes as available antigens in living neuronal membranes and supplies proof-of-principle that anti-ganglioside-complex antibodies in sera from GBS patients can induce complement-mediated damage. This strongly supports the hypothesis that autoimmune targeting of ganglioside-complexes is of pathogenic relevance in a proportion of GBS patients

Libraries and open society; Popper, Soros and digital information

This paper examines the role of libraries and information services, in promoting the ‘open society’ espoused by Karl Popper and George Soros. After a brief discussion of the nature of an ‘open society’, the paper covers the role played by provision of knowledge and information, of new technology, particularly the Internet, and of critical thinking and digital literacy in the development of this form of society. Conclusions are drawn for the role of libraries and librarians, with seven general principles suggested: • provision of access to a wide variety of sources without ‘negative’ restriction or censorship • provision of ‘positive’ guidance on sources, based on open and objective criteria • a recognition that a ‘free flow of information’ though essential, is not sufficient • a recognition that provision of factual information, while valuable, is not enough • a need for a specific concern for the effect of new ICTs, and the Internet in particular • promotion of critical thinking and digital literacy • a need for explicit consideration of the ethical values of librarie

Contactin-1 and Neurofascin-155/-186 Are Not Targets of Auto-Antibodies in Multifocal Motor Neuropathy

Multifocal motor neuropathy is an immune mediated disease presenting with multifocal muscle weakness and conduction block. IgM auto-antibodies against the ganglioside GM1 are detectable in about 50% of the patients. Auto-antibodies against the paranodal proteins contactin-1 and neurofascin-155 and the nodal protein neurofascin-186 have been detected in subgroups of patients with chronic inflammatory demyelinating polyneuropathy. Recently, auto-antibodies against neurofascin-186 and gliomedin were described in more than 60% of patients with multifocal motor neuropathy. In the current study, we aimed to validate this finding, using a combination of different assays for auto-antibody detection. In addition we intended to detect further auto-antibodies against paranodal proteins, specifically contactin-1 and neurofascin-155 in multifocal motor neuropathy patients’ sera. We analyzed sera of 33 patients with well-characterized multifocal motor neuropathy for IgM or IgG anti-contactin-1, anti-neurofascin-155 or -186 antibodies using enzyme-linked immunosorbent assay, binding assays with transfected human embryonic kidney 293 cells and murine teased fibers. We did not detect any IgM or IgG auto-antibodies against contactin-1, neurofascin-155 or -186 in any of our multifocal motor neuropathy patients. We conclude that auto-antibodies against contactin-1, neurofascin-155 and -186 do not play a relevant role in the pathogenesis in this cohort with multifocal motor neuropathy

Frequency and time to relapse after discontinuing 6-month therapy with IVIg or pulsed methylprednisolone in CIDP

Background: We reported that 6-month therapy with intravenous immunoglobulin (IVIg) was more frequently effective or tolerated than intravenous methylprednisolone (IVMP) in patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). We now retrospectively compared the proportion of patients who eventually worsened after discontinuing therapy and the median time to clinical worsening. Methods: By March 2013, data were available from 41 of the 45 patients completing the trial with a median follow-up after therapy discontinuation of 42 months (range 1-60). Three patients withdrew during the original study and one failed to respond to either of the therapies. No patient received a diagnosis alternative to CIDP during the follow-up. Results: Twenty-eight of the 32 patients treated with IVIg (as primary or secondary therapy after failing to respond to IVMP) improved after therapy (87.5%) as compared with 13 of the 24 patients treated with IVMP as primary or secondary therapy (54.2%). After a median follow-up of 42 months (range 1-57), 24 out of 28 patients responsive to IVIg (85.7%) worsened after therapy discontinuation. The same occurred in 10 out of 13 patients (76.9%) responsive to IVMP (p=0.659) after a median follow-up of 43 months (range 7-60). Worsening occurred 1-24 months (median 4.5) after IVIg discontinuation and 1-31 months (median 14) after IVMP discontinuation (p=0.0126). Conclusions: A similarly high proportion of patients treated with IVIg or IVMP eventually relapse after therapy discontinuation but the median time to relapse was significantly longer after IVMP than IVIg. This difference may help to balance the more frequent response to IVIg than to IVMP in patients with CIDP