El triacetato de celulosa asimétrico es una alternativa segura y eficaz para la hemodiafiltración en línea

Background

In post-dilution haemodiafiltration only synthetic membranes have been used to date. Asymmetric cellulose triacetate (ATA?) is now available, whose characteristics are suitable for this technique.

The non glycanated endocan polypeptide slows tumor growth by inducing stromal inflammatory reaction

Endocan expression is increasingly studied in various human cancers. Experimental evidence showed that human endocan, through its glycan chain, is implicated in various processes of tumor growth. We functionally characterize mouse endocan which is also a chondroitin sulfate proteoglycan but much less glycanated than human endocan. Distant domains from the O-glycanation site, located within exons 1 and 2 determine the glycanation pattern of endocan. In opposite to the human homologue, overexpression of mouse endocan in HT-29 cells delayed the tumor appearance and reduced the tumor growth rate. This tumor growth inhibition is supported by non glycanated form of mouse endocan. Non glycanated human endocan overexpressed in HT-29, A549 or K1000 cells also exhibited an anti-tumor effect. Moreover, systemic delivery of non glycanated human endocan also results in HT-29 tumor growth delay. In vitro, endocan polypeptide did not affect HT-29 cell proliferation, nor cell viability. In tumor tissue sections, a stromal inflammatory reaction was observed only in tumors overexpressing endocan polypeptide, and depletion of CD122+ cells was able to delete partially the anti-tumor effect of endocan polypeptide. These results reveal a novel pathway for endocan in the control of tumor growth, which involves inflammatory cells of the innate immunity.     

Recovery of aphasia after stroke: a 1-year follow-up study

Semantics, phonology, and syntax are essential elements of aphasia diagnosis and treatment. Until now, these linguistic components have not been specifically addressed in follow-up studies of aphasia recovery after stroke. The aim of this observational prospective follow-up study was to investigate semantic, phonological, and syntactic recovery in aphasic stroke patients. In addition, we investigated the recovery of verbal communication and of aphasia severity. We assessed 147 aphasic patients at 1, 2, and 6 weeks, 3 and 6 months, and 1 year after stroke with the ScreeLing, a screening test for detecting deficits on the three main linguistic components, the aphasia severity rating scale (ASRS), a measure of verbal communication, and the Token test, a measure of aphasia severity. We investigated the differences in scores between the six time points with mixed models. Semantics and syntax improved up to 6 weeks (p < 0.001) after stroke, and phonology up to 3 months (p ≤ 0.001). ASRS improved up to 6 months (p < 0.05) and the Token test up to 3 months (p < 0.001). We conclude that in aphasia after stroke, various linguistic components have a different recovery pattern, with phonology showing the longest period of recovery that paralleled aphasia severity, as measured with the Token test. The improvement of verbal communication continues after the stabilization of the recovery of the linguistic components.     

Splicing factor TRA2B is required for neural progenitor survival

Alternative splicing of pre‐mRNAs can rapidly regulate the expression of large groups of proteins. The RNA binding protein TRA2B (SFRS10) plays well‐established roles in developmentally regulated alternative splicing during Drosophila sexual differentiation. TRA2B is also essential for mammalian embryogenesis and is implicated in numerous human diseases. Precise regulation of alternative splicing is critical to the development and function of the central nervous system; however, the requirements for specific splicing factors in neurogenesis are poorly understood. This study focuses on the role of TRA2B in mammalian brain development. We show that, during murine cortical neurogenesis, TRA2B is expressed in both neural progenitors and cortical projection neurons. Using cortex‐specific Tra2b mutant mice, we show that TRA2B depletion results in apoptosis of the neural progenitor cells as well as disorganization of the cortical plate. Thus, TRA2B is essential for proper development of the cerebral cortex. J. Comp. Neurol. 522:372–392, 2014. © 2013 Wiley Periodicals, Inc.