Presence of new mecA and mph(C) variants conferring antibiotic resistance in Staphylococcus spp. isolated from the skin of horses before and after clinic admission

Because of the frequency of multiple antibiotic resistance, Staphylococcus species often represent a challenge in incisional infections of horses undergoing colic surgery. To investigate the evolution of antibiotic resistance patterns before and after preventative peri- and postoperative penicillin treatment, staphylococci were isolated from skin and wound samples at different times during hospitalization. Most staphylococci were normal skin commensals and belonged to the common coagulase-negative group. In some cases they turned out to be opportunistic pathogens present in wound infections. MICs were determined for 12 antibiotics, and antibiotic resistance genes were detected by microarray. At hospital admission, horses harbored staphylococci that were susceptible to antibiotics or resistant to one group of drugs, mainly due to the presence of new variants of the methicillin and macrolide resistance genes mecA and mph(C), respectively. After 3 days, the percentage of Staphylococcus isolates displaying antibiotic resistance, as well as the number of resistance genes per isolate, increased moderately in hospitalized horses without surgery or penicillin treatment but dramatically in hospitalized horses after colic surgery as well as penicillin treatment. Staphylococcus species displaying multiple resistance were found to harbor mainly genes conferring resistance to beta-lactams (mecA and blaZ), aminoglycosides [str and aac(6')-Ie-aph(2')-Ia], and trimethoprim [dfr(A) and dfr(D)]. Additional genes conferring resistance to macrolides [mph(C), erm(C), and erm(B)], tetracycline [tet(K) and tet(M)], chloramphenicol [cat(pC221) and cat(pC223)], and streptothricin (sat4) appeared in several strains. Hospitalization and preventive penicillin use were shown to act as selection agents for multidrug-resistant commensal staphylococcal flora.

Disseminated and sustained HIV infection in CD34+ cord blood cell-transplanted Rag2-/-gamma c-/- mice

Because of species selectivity, HIV research is largely restricted to in vitro or clinical studies, both limited in their ability to rapidly assess new strategies to fight the virus. To prospectively study some aspects of HIV in vivo, immunodeficient mice, transplanted with either human peripheral blood leukocytes or human fetal tissues, have been developed. Although these are susceptible to HIV infection, xenoreactivity, and short infection spans, resource and ethical constraints, as well as biased HIV coreceptor tropic strain infection, pose substantial problems in their use. Rag2(-/-)gamma(c)(-/-) mice, transplanted as newborns with human CD34(+) cells, were recently shown to develop human B, T, and dendritic cells, constituting lymphoid organs in situ. Here we tested these mice as a model system for HIV-1 infection. HIV RNA levels peaked to up to 2 x 10(6) copies per milliliter of plasma early after infection, and viremia was observed for up to 190 days, the longest time followed. A marked relative CD4(+) T cell depletion in peripheral blood occurred in CXCR4-tropic strain-infected mice, whereas this was less pronounced in CCR5-tropic strain-infected animals. Thymus infection was almost exclusively observed in CXCR4-tropic strain-infected mice, whereas spleen and lymph node HIV infection occurred irrespective of coreceptor selectivity, consistent with respective coreceptor expression on human CD4(+) T cells. Thus, this straightforward to generate and cost-effective in vivo model closely resembles HIV infection in man and therefore should be valuable to study virus-induced pathology and to rapidly evaluate new approaches aiming to prevent or treat HIV infection.

Echicetin, a GPIb-binding snake C-type lectin from Echis carinatus, also contains a binding site for IgMkappa responsible for platelet agglutination in plasma and inducing signal transduction

Echicetin, a heterodimeric snake C-type lectin from Echis carinatus, is known to bind specifically to platelet glycoprotein (GP)Ib. We now show that, in addition, it agglutinates platelets in plasma and induces platelet signal transduction. The agglutination is caused by binding to a specific protein in plasma. The protein was isolated from plasma and shown to cause platelet agglutination when added to washed platelets in the presence of echicetin. It was identified as immunoglobulin Mkappa (IgMkappa) by peptide sequencing and dot blotting with specific heavy and light chain anti-immunoglobulin reagents. Platelet agglutination by clustering echicetin with IgMkappa induced P-selectin expression and activation of GPIIb/IIIa as well as tyrosine phosphorylation of several signal transduction molecules, including p53/56(LYN), p64, p72(SYK), p70 to p90, and p120. However, neither ethylenediaminetetraacetic acid nor specific inhibition of GPIIb/IIIa affected platelet agglutination or activation by echicetin. Platelet agglutination and induction of signal transduction could also be produced by cross-linking biotinylated echicetin with avidin. These data indicate that clustering of GPIb alone is sufficient to activate platelets. In vivo, echicetin probably activates platelets rather than inhibits platelet activation, as previously proposed, accounting for the observed induction of thrombocytopenia.

Mechano-regulated tenascin-C orchestrates muscle repair

Tenascin-C (TNC) is a mechano-regulated, morphogenic, extracellular matrix protein that is associated with tissue remodeling. The physiological role of TNC remains unclear because transgenic mice engineered for a TNC deficiency, via a defect in TNC secretion, show no major pathologies. We hypothesized that TNC-deficient mice would demonstrate defects in the repair of damaged leg muscles, which would be of functional significance because this tissue is subjected to frequent cycles of mechanical damage and regeneration. TNC-deficient mice demonstrated a blunted expression of the large TNC isoform and a selective atrophy of fast-muscle fibers associated with a defective, fast myogenic expression response to a damaging mechanical challenge. Transcript profiling mapped a set of de-adhesion, angiogenesis, and wound healing regulators as TNC expression targets in striated muscle. Expression of these regulators correlated with the residual expression of a damage-related 200-kDa protein, which resembled the small TNC isoform. Somatic knockin of TNC in fast-muscle fibers confirmed the activation of a complex expression program of interstitial and slow myofiber repair by myofiber-derived TNC. The results presented here show that a TNC-orchestrated molecular pathway integrates muscle repair into the load-dependent control of the striated muscle phenotype.

The Protein-tyrosine-phosphatase SHP2 is phosphorylated on serine residues 576 and 591 by protein kinase C isoforms alpha, beta 1, beta 2, and eta

To study whether protein kinase C (PKC) isoforms can interact with protein-tyrosine-phosphatases (PTPs) which are connected to the insulin signaling pathway, we co-overexpressed PKC isoforms together with insulin receptor, docking proteins, and the PTPs SHP1 and SHP2 in human embryonic kidney (HEK) 293 cells. After phorbol ester induced activation of PKC isoforms alpha, beta 1, beta 2, and eta, we could show a defined gel mobility shift of SHP2, indicating phosphorylation on serine/threonine residues. This phosphorylation was not dependent on insulin receptor or insulin receptor substrate-1 (IRS-1) overexpression and did not occur for the closely related phosphatase SHP1. Furthermore, PKC phosphorylation of SHP2 was completely blocked by the PKC inhibitor bisindolylmaleimide and was not detectable when SHP2 was co-overexpressed with kinase negative mutants of PKC beta 1 and -beta 2. The phosphorylation also occurred on endogenous SHP2 in Chinese hamster ovary (CHO) cells stably overexpressing PKC beta 2. Using point mutants of SHP2, we identified serine residues 576 and 591 as phosphorylation sites for PKC. However, no change of phosphatase activity by TPA treatment was detected in an in vitro assay. In summary, SHP2 is phosphorylated on serine residues 576 and 591 by PKC isoforms alpha, beta 1, beta 2, and eta.

¿Presencia del español en el paisaje urbano de Washington D.F.? Un estudio del paisaje lingüístico mediado por Internet

Objetivo de esta comunicación es presentar los resultados sobre un análisis realizado en torno a lo que podemos denominar el «paisaje lingüístico hispano virtual» en Washington D.F. Los estudios sobre paisaje lingüístico han experimentado en el último tiempo un verdadero boom, sobre todo como reflejo de la convivencia de diferentes culturas con sus respectivas lenguas y variedades en las urbes del siglo XXI. En efecto: el paisaje lingüístico multilingüe es uno de los aspectos más explotados en trabajos en esta línea teórica. En este estudio el centro de atención no es el paisaje "real", documentado in situ y captado motu propio en instantáneas por nuestros aparatos fotográficos, sino el paisaje lingüístico mediatizado por el ordenador y difundido mediante la World Wide Web. En este sentido, lo que nos interesa es si se ve reflejada y qué manera la hispanidad en Washington D.F. a través del paisaje urbano que nos ofrecen programas especializados como Google Earth y Google Street View. Con este objetivo proponemos un paseo virtual por Washington D.F. y sus diferentes barrios para analizar mediante un estudio de naturaleza cuantitativa y cualitativa, apoyándonos en las herramientas teóricas y metodológicas que ofrecen los estudios de paisaje lingüístico y de la Comunicación Mediada por Ordenadores, de qué manera lo hispano constituye un engranaje del paisaje lingüístico de esta ciudad.

Israels Heiligthum in der Gegenwart : Predigt gehalten in der Synagoge zu Hannover am Sonnabend, den 10. Februar 1883

von I. Prager

Literatura, prensa periódica y público lector en los procesos de nacionalización de la cultura en Argentina y en Chile (1828-1863)

La tesis indaga las relaciones entre prensa periódica y cultura literaria que durante la primera mitad del siglo XIX, tanto en Chile como en el Río de la Plata, viabilizaron los procesos de formación de un imaginario y un público lector nacionales, y contribuyeron a la creación -temporal y territorialmente diferenciada- de un canon literario y estético. La tesis analiza las modalidades de construcción pública de las culturas literarias chilena y argentina ya consolidada la independencia, y especialmente los modos en que la prensa periódica incidió en los programas literarios de las respectivas élites letradas. Para ello, se estudia un amplio corpus de publicaciones periódicas que se extiende desde El Recopilador (1836) hasta El Talismán o El Corsario (1840) en el Río de la Plata, y desde El Semanario de Santiago (1842) hasta El Correo Literario (1858) o La Semana (1859) en Chile. Los límites de la periodización propuesta acompañan el itinerario de esas publicaciones de la primera mitad del siglo, y coinciden con el ingreso y la difusión de las ideas románticas que incentivaron la preocupación letrada por definir la problemática relación entre cultura y nacionalidad. El enfoque comparativo, por su parte, contempla particularidades, así como simetrías y divergencias, en la formación de imaginarios y tradiciones culturales de ambos territorios.

Jorge M. Machetta y Claudia D'Amico (editores). El problema del conocimiento en Nicolás de Cusa: genealogía y proyecciones. Buenos Aires, Biblos, 2005, 445 pp.

Fil: Garay, Diego. Universidad Nacional de La Plata. Facultad de Humanidades y Ciencias de la Educación; Argentina.