The evolution of the public sphere

Purpose: The purpose of this study is to rethink the issue of publicity from a cross-cultural and evolutionary perspective. Design/methodology/approach: Assuming that there is a dominant paradigm in the studies of the public sphere centered on Habermas’ ideas, media theory (and especially Luhmann who is considered as a media theorist) is selected as a new context that provides different concepts, ideas, language games and metaphors that allow the re-foundation of the study of publicity. Findings: Publicity as a social structure emerges – and acquires different forms during history – out of the complex dynamics resulting from the interaction between success media, such as power, and different kinds of dissemination media. Originality/value: A research into the forms of publicity not only promotes awareness of the ubiquity of the phenomenon across cultural evolution, but also offers tools to make new discoveries and systematize what is already known about the subject and its ramifications.Fil: Blanco Rivero, José Javier. Universidad Nacional de Quilmes. Departamento de Ciencias Sociales. Centro de Historia Intelectual; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Mediality, temporality, social cognition, and evolution

In the literature of Media Studies, the word mediality has emerged as an expression of the concern about the specificity of media and their link to time, experience, technology and social change. However, mediality is not yet a concept, since the description of the function of media as mediation and transmission has become an obstacle to achieve further developments. In light of these remarks, this paper proposes a theoretical arrangement that gives meaning to mediality by connecting the word into a network of concepts, such as social cognition, evolution, temporality, synchronization and double closure. In order to achieve this goal, the author designs a theoretical apparatus consisting of the self-referential coupling between N. Luhmann’s systems theory, H. von Foerster’s second order cybernetics, R. Harris’ integration linguistics, and A. Clark’s extended cognition. A consistent integration and interpretation of the sketched theory, allows us to draw the conclusion that in order to comprehend mediality, it is crucial to understand the relationship between information, double closure, social cognition and evolution, while questions regarding human cognition do not be to be involved; and if that should be the case, research should depart from the problem of the structural coupling between human and social cognition.Fil: Blanco Rivero, José Javier. Universidad Nacional de Quilmes. Departamento de Ciencias Sociales. Centro de Historia Intelectual; Argentina. Universidad Simón Bolívar; Venezuela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Efecto de las hormonas sexuales masculinas en la respuesta vasomotora inducida por estimulación eléctrica y acetilcolina en arteria mesentérica de rata: papel de la proteína kinasa C

Tesis doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Medicina. Departamento de Fisiología. Fecha de lectura: 22 de Junio de 200

Historia conceptual y social del totalitarismo. Una propuesta teórico-metodológica

Nuestro objetivo es formular una propuesta teórico-metodológica para el estudio de la historia intelectual, capaz de explicar las interrelaciones entre cambio social y cambio lingüístico, traduciendo tales reflexiones en herramientas para la investigación histórica. Para tal fin, tomamos la distinción semántica/estructura social, elaborada por la sociología del conocimiento de Niklas Luhmann y la redescribimos introduciendo la distinción entre información y significado. El mencionado marco teórico es puesto a prueba realizando un bosquejo de la historia conceptual y social del totalitarismo. Llegamos a la conclusión de que el concepto de totalitarismo nos permite dar cuenta de cómo los significados se autoorganizan siguiendo una dinámica histórica propia, aunque ninguna producción de significado puede tener lugar fuera de los sistemas sociales y de los códigos que éstos emplean para procesar información. La historia intelectual se escribe simultáneamente sobre los dos registros de la información y el significado

The Wound-Healing Portal Hypertensive Response

Portal hypertensive inflammation is associated with chronic liver diseases. The three successive and overlapping systemic inflammatory phenotypes, i.e., neurogenic, immune, and endocrine, which characterize the wound-healing response, are expressed by the portal venous system upon liver injury. The diverse functions of hepatic stellate cells in homeostasis and inflammation indicate the versatile nature of these mesenchymal-derived cells, which could adopt numerous phenotypes according to the interstitial microenvironmental characteristics. Consequently, these inflammatory phenotypes could represent the reexpression of two extra-embryonic functional axis, i.e., coelomic-amniotic and trophoblastic-vitelline, whose coupling in the portal system would induce a gastrulation-related phenotype. Therefore, hepatic stellate cells and liver-specific mesenchymal cells could recapitulate and couple these abovementioned extra-embryonic phenotypes during portal hypertension. These hepatic cellular population, thanks to their potential ability to integrate and reexpress functions showing analogies to extra-embryonic functions, display characteristics of stem/progenitor cells. In this way, during the development of portal hypertension, hepatic stellate cells not only could reexpress extra-embryonic functions, but also could adapt themselves in order to induce a gastrulation-related process in the space of Disse. Hence, by understanding the ontogenic interactions between hepatic stellate cells and the host inflammatory response in portal hypertension, it is possible to design effective therapeutic and prophylactic strategies to avoid or reverse wound-like hypertensive response

Impacto de la transposición de la Directiva de Servicios en Castilla y León

[ES]El presente estudio recoge los trabajos elaborados por el grupo de investigación constituido con motivo de la convocatoria del Premio «Colección de Estudios del Consejo Económico y Social de Castilla y León» (edición 2009-II)

Beneficial effect of a multistrain synbiotic prodefen® plus on the systemic and vascular alterations associated with metabolic syndrome in rats: The role of the neuronal nitric oxide synthase and protein kinase A

A high fat diet (HFD) intake is crucial for the development and progression of metabolic syndrome (MtS). Increasing evidence links gut dysbiosis with the metabolic and vascular alterations associated with MtS. Here we studied the use of a combination of various probiotic strains together with a prebiotic (synbiotic) in a commercially available Prodefen® Plus. MtS was induced by HFD (45%) in maleWistar rats. Half of the MtS animals received Prodefen® Plus for 4 weeks. At 12 weeks, we observed an increase in body weight, together with the presence of insulin resistance, liver steatosis, hypertriglyceridemia and hypertension in MtS rats. Prodefen® Plus supplementation did not a ect the body weight gain but ameliorated all the MtS-related symptoms. Moreover, the hypertension induced by HFD is caused by a diminished both nitric oxide (NO) functional role and release probably due to a diminished neuronal nitric oxide synthase (nNOS) activation by protein kinase A (PKA) pathway. Prodefen® Plus supplementation for 4 weeks recovered the NO function and release and the systolic blood pressure was returned to normotensive values as a result. Overall, supplementation with Prodefen® Plus could be considered an interesting non-pharmacological approach in MtS.This research was funded by Italfarmaco, S.A (L.O.U. 83; 0138/2018), CiberCV (Grant number: CB16/11/00286), the European Regional Development Grant (FEDER) (Comunidad de Madrid, Grant number B2017/BMD-3676), and R + D projects for young researchers, Universidad Autónoma de Madrid (Comunidad de Madrid (SI1-PJI-2019-00321). R.R.-D. received a fellowship from Juan de la Cierva Program (IJCI-2017-31399)

Acute-on-chronic liver disease enhances phenylephrine-induced endothelial nitric oxide release in rat mesenteric resistance arteries through enhanced PKA, PI3K/AKT and cGMP signalling pathways

Acute-on-chronic liver disease is a clinical syndrome characterized by decompensated liver fibrosis, portal hypertension and splanchnic hyperdynamic circulation. We aimed to determine whether the alpha-1 agonist phenylephrine (Phe) facilitates endothelial nitric oxide (NO) release by mesenteric resistance arteries (MRA) in rats subjected to an experimental microsurgical obstructive liver cholestasis model (LC). Sham-operated (SO) and LC rats were maintained for eight postoperative weeks. Phe-induced vasoconstriction (in the presence/absence of the NO synthase –NOS- inhibitor L-NAME) and vasodilator response to NO donor DEA-NO were analysed. Phe-induced NO release was determined in the presence/absence of either H89 (protein kinase –PK- A inhibitor) or LY 294002 (PI3K inhibitor). PKA and PKG activities, alpha-1 adrenoceptor, endothelial NOS (eNOS), PI3K, AKT and soluble guanylate cyclase (sGC) subunit expressions, as well as eNOS and AKT phosphorylation, were determined. The results show that LC blunted Phe-induced vasoconstriction, and enhanced DEA-NO-induced vasodilation. L-NAME increased the Phe-induced contraction largely in LC animals. The Phe-induced NO release was greater in MRA from LC animals. Both H89 and LY 294002 reduced NO release in LC. Alpha-1 adrenoceptor, eNOS, PI3K and AKT expressions were unchanged, but sGC subunit expression, eNOS and AKT phosphorylation and the activities of PKA and PKG were higher in MRA from LC animals. In summary, these mechanisms may help maintaining splanchnic vasodilation and hypotension observed in decompensated LC.This study was supported by Ministerio de Economía y Competitividad (SAF2012-38530), CiberCV (CB16/11/00286 and CB16/11/00264), and Fondo Europeo de Desarrollo Regional (FEDER) a way to build Europe, Comunidad de Madrid (B2017/BMD-3676

A blunted sympathetic function and an enhanced nitrergic activity contribute to reduce mesenteric resistance in hyperthyroidism

We aimed to determine whether an experimental model of hyperthyroidism could alter the function of sympathetic and nitrergic components of mesenteric innervation. For this purpose, male Wistar rats were divided into (1) control rats (CT) and (2) rats infused with L-Thyroxine (HT). Body weight gain and adipose tissue accumulation were lower in HT rats, while systolic blood pressure and citrate synthase activity in the soleus muscle were increased by HT. In segments from the superior mesenteric artery, the application of an electrical field stimulation (EFS) induced a vasoconstrictor response, which was lower in arteries from HT animals. The alpha-adrenoceptor antagonist phentolamine diminished EFS-induced vasoconstriction to a lower extent in HT arter-ies, while the purinergic receptor antagonist suramin reduced contractile response to EFS only in segments from CT. In line with this, noradrenaline release, tyrosine hydroxylase expression and activation and dopamine β hydroxylase expression were diminished in HT. The unspecific nitric oxide synthase (NOS) inhibitor L-NAME increased EFS-induced vasoconstriction more markedly in segments from HT rats. NO release was enhanced in HT, probably due to an enhancement in neuronal NOS activity, in which a hyperactivation of both PKC and PI3K-AKT signaling pathways might play a relevant role. In conclusion, perivascular mesenteric innervation might contribute to reduce the vascular resistance observed in hyperthyroidism.This research was funded by CiberCV (Grant number: CB16/11/00286), the European Regional Development Grant (FEDER) (Comunidad de Madrid, Grant number B2017/BMD-3676), Ministerio de Economía, Industria y Competitividad (SAF 2016-80905-P) and R + D projects for young researchers, Universidad Autónoma de Madrid (Comunidad de Madrid (SI1-PJI-2019-00321)

Construction, purification, and characterization of a chimeric TH1 antagonist

BACKGROUND: TH1 immune response antagonism is a desirable approach to mitigate some autoimmune and inflammatory reactions during the course of several diseases where IL-2 and IFN-γ are two central players. Therefore, the neutralization of both cytokines could provide beneficial effects in patients suffering from autoimmune or inflammatory illnesses. RESULTS: A chimeric antagonist that can antagonize the action of TH1 immunity mediators, IFN-γ and IL-2, was designed, engineered, expressed in E. coli, purified and evaluated for its in vitro biological activities. The TH1 antagonist molecule consists of the extracellular region for the human IFNγ receptor chain 1 fused by a four-aminoacid linker peptide to human 60 N-terminal aminoacid residues of IL-2. The corresponding gene fragments were isolated by RT-PCR and cloned in the pTPV-1 vector. E. coli (W3110 strain) was transformed with this vector. The chimeric protein was expressed at high level as inclusion bodies. The protein was partially purified by pelleting and washing. It was then solubilized with strong denaturant and finally refolded by gel filtration. In vitro biological activity of chimera was demonstrated by inhibition of IFN-γ-dependent HLA-DR expression in Colo 205 cells, inhibition of IFN-γ antiproliferative effect on HEp-2 cells, and by a bidirectional effect in assays for IL-2 T-cell dependent proliferation: agonism in the absence versus inhibition in the presence of IL-2. CONCLUSION: TH1 antagonist is a chimeric protein that inhibits the in vitro biological activities of human IFN-γ, and is a partial agonist/antagonist of human IL-2. With these attributes, the chimera has the potential to offer a new opportunity for the treatment of autoimmune and inflammatory diseases