Protein phosphatase inhibition assays for okadaic acid detection in shellfish: matrix effects, applicability and comparison with LC-MS/MS analysis

The applicability of the protein phosphatase inhibition assay (PPIA) to the determination of okadaic acid (OA) and its acyl derivatives in shellfish samples has been investigated, using a recombinant PP2A and a commercial one. Mediterranean mussel, wedge clam, Pacific oyster and flat oyster have been chosen as model species. Shellfish matrix loading limits for the PPIA have been established, according to the shellfish species and the enzyme source. A synergistic inhibitory effect has been observed in the presence of OA and shellfish matrix, which has been overcome by the application of a correction factor (0.48). Finally, Mediterranean mussel samples obtained from Rı´a de Arousa during a DSP closure associated to Dinophysis acuminata, determined as positive by the mouse bioassay, have been analysed with the PPIAs. The OA equivalent contents provided by the PPIAs correlate satisfactorily with those obtained by liquid chromatography–tandem mass spectrometry (LC–MS/MS).

Amelioration of Duchenne muscular dystrophy in mdx mice by elimination of matrix-associated fibrin-driven inflammation coupled to the αMβ2 leukocyte integrin receptor

In Duchenne muscular dystrophy (DMD), a persistently altered and reorganizing extracellular matrix (ECM) within inflamed muscle promotes damage and dysfunction. However, the molecular determinants of the ECM that mediate inflammatory changes and faulty tissue reorganization remain poorly defined. Here, we show that fibrin deposition is a conspicuous consequence of muscle-vascular damage in dystrophic muscles of DMD patients and mdx mice and that elimination of fibrin(ogen) attenuated dystrophy progression in mdx mice. These benefits appear to be tied to: (i) a decrease in leukocyte integrin α(M)β(2)-mediated proinflammatory programs, thereby attenuating counterproductive inflammation and muscle degeneration; and (ii) a release of satellite cells from persistent inhibitory signals, thereby promoting regeneration. Remarkably, Fib-gamma(390-396A) (Fibγ(390-396A)) mice expressing a mutant form of fibrinogen with normal clotting function, but lacking the α(M)β(2) binding motif, ameliorated dystrophic pathology. Delivery of a fibrinogen/α(M)β(2) blocking peptide was similarly beneficial. Conversely, intramuscular fibrinogen delivery sufficed to induce inflammation and degeneration in fibrinogen-null mice. Thus, local fibrin(ogen) deposition drives dystrophic muscle inflammation and dysfunction, and disruption of fibrin(ogen)-α(M)β(2) interactions may provide a novel strategy for DMD treatment.

New predictions for inclusive heavy-quarkonium P-wave decays

We show that some nonrelativistic quantum chromodynamics color-octet matrix elements can be written in terms of (derivatives of) wave functions at the origin and of nonperturbative universal constants once the factorization between the soft and ultrasoft scales is achieved by using an effective field theory where only ultrasoft degrees of freedom are kept as dynamical entities. This allows us to derive a new set of relations between inclusive heavy-quarkonium P-wave decays into light hadrons with different principal quantum numbers and with different heavy flavors. In particular, we can estimate the ratios of the decay widths of bottomonium P-wave states from charmonium data.

New predictions for inclusive heavy-quarkonium p-wave decays

We show that some nonrelativistic quantum chromodynamics color-octet matrix elements can be written in terms of (derivatives of) wave functions at the origin and of nonperturbative universal constants once the factorization between the soft and ultrasoft scales is achieved by using an effective field theory where only ultrasoft degrees of freedom are kept as dynamical entities. This allows us to derive a new set of relations between inclusive heavy-quarkonium P-wave decays into light hadrons with different principal quantum numbers and with different heavy flavors. In particular, we can estimate the ratios of the decay widths of bottomonium P-wave states from charmonium data.

Capitals, trajectòries i estratègies: la teoria general dels camps de P. Bourdieu

El model de classes de P. Bourdieu articula la dimensió objectiva —l’estructura de classe— i la dimensió subjectiva —l’acció de classe—. Aquesta anàlisi de classe forma part d’un debat al voltant de la naturalesa de la realitat social, en el qual el punt més important és la connexió del camp de la producció i del camp de la reproducció de subjectes. Bourdieu, en enfasitzar la condició relacional de l’àmbit social, defineix l’acció social com a dependent de l’estructura relacional, en existir una connexió lògica necessària entre la localització dels agents en un conjunt de relacions socials i els seus interessos, objectius i estratègies d’acció. Per tant, per a aquest autor, hi ha una eficàcia estructuradora de l’acció dels agents socials per l’estructura de classe, i es constitueix, així, en una matriu d’acció, o millor dit, en una estructura probabilística de l’acció. És, doncs, fonamental, considerar el paper de l’acció en la construcció de les classes en si, ja que les classes teòriques, agrupacions fictícies que només existeixen sobre el paper, estan predisposades a convertir-se en classes en el sentit marxista del terme. I sols es passa de la classe sobre el paper a clase real a costa d’una labor política de movilització. Així, l’existència de classes, tant en la teoria com en la realitat, és una aposta de lluites en existir un espai social, un espai de diferències, en el qual les classes existeixen en estat virtual, no com quelcom donat, sinó com quelcom que es tracta de construir.

Planarians as a model to assess in vivo the role of matrix metalloproteinase genes during homeostasis and regeneration

Matrix metalloproteinases (MMPs) are major executors of extracellular matrix remodeling and, consequently, play key roles in the response of cells to their microenvironment. The experimentally accessible stem cell population and the robust regenerative capabilities of planarians offer an ideal model to study how modulation of the proteolytic system in the extracellular environment affects cell behavior in vivo. Genome-wide identification of Schmidtea mediterranea MMPs reveals that planarians possess four mmp-like genes. Two of them (mmp1 and mmp2) are strongly expressed in a subset of secretory cells and encode putative matrilysins. The other genes (mt-mmpA and mt-mmpB) are widely expressed in postmitotic cells and appear structurally related to membrane-type MMPs. These genes are conserved in the planarian Dugesia japonica. Here we explore the role of the planarian mmp genes by RNA interference (RNAi) during tissue homeostasis and regeneration. Our analyses identify essential functions for two of them. Following inhibition of mmp1 planarians display dramatic disruption of tissues architecture and significant decrease in cell death. These results suggest that mmp1 controls tissue turnover, modulating survival of postmitotic cells. Unexpectedly, the ability to regenerate is unaffected by mmp1(RNAi). Silencing of mt-mmpA alters tissue integrity and delays blastema growth, without affecting proliferation of stem cells. Our data support the possibility that the activity of this protease modulates cell migration and regulates anoikis, with a consequent pivotal role in tissue homeostasis and regeneration. Our data provide evidence of the involvement of specific MMPs in tissue homeostasis and regeneration and demonstrate that the behavior of planarian stem cells is critically dependent on the microenvironment surrounding these cells. Studying MMPs function in the planarian model provides evidence on how individual proteases work in vivo in adult tissues. These results have high potential to generate significant information for development of regenerative and anti cancer therapies.

Finite-temperature T matrix in a real-time formalism

A generalized off-shell unitarity relation for the two-body scattering T matrix in a many-body medium at finite temperature is derived, through a consistent real-time perturbation expansion by means of Feynman diagrams. We comment on perturbation schemes at finite temperature in connection with an erroneous formulation of the Dyson equation in a paper recently published.