Importancia de la tecnología en el aprendizaje de la producción animal.

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Análisis de las distintas competencias sociales demandadas por el mercado laboral al profesional de las ciencias veterinarias

Las competencias sociales son requisitos cada vez más ponderados en el currículum y en la formación integral del médico veterinario. La capacidad para el trabajo en equipo, la confianza en sí mismo y en los demás, la capacidad para comunicarse, etc., son conductas que, en un contexto interpersonal, le permiten expresar sus sentimientos, opiniones o derechos de un modo adecuado a la situación, ayudándolo en la resolución de conflictos inmediatos, mientras minimiza la probabilidad de futuros problemas ante una sociedad cada vez más exigente.A partir del marco teórico, para el cual se reunió abundante información respecto a qué son las “competencias o habilidades sociales” y qué importancia fueron adquiriendo en estos últimos tiempos, se planteó el interrogante acerca de cuáles son las que demanda hoy el mercado laboral para el Profesional Veterinario. Para ello se analizaron diversas solicitudes de empleos por parte de empresas de insumos y productos agrícolas, industrias afines, productores ganaderos, y otros posibles empleadores; generando un orden de valoración de las competencias más apuntadas como requisitos para acceder a la oferta de trabajo. A partir del orden previamente citado, confeccionamos encuestas de fácil ejecución y análisis, con el fin de analizar objetivamente de dicha valoración.Nuestro trabajo tiene como objetivo principal evidenciar la valoración de las competencias sociales por parte del mercado laboral, como parte de una herramienta que tiene como fin argumentar la importancia de la inserción de estas competencias en la educación y formación del futuro profesional, generando el debate a nivel institucional

Evaluación de competencias orales: un aporte a la evaluación tradicional de los aprendizajes

Actualmente, siguen empleándose métodos de enseñanza y evaluación de la Matemática que enfatizan el manejo conceptual y procedimental, donde el alumno debe resolver problemas estándar en un determinado tiempo. Esta visión no considera importantes variables que influyen en el proceso educativo.Para modificar esto, es preciso presentar la matemática enmarcada en situaciones reales que alienten al estudiante, desafiando su interés. En la Facultad de Veterinaria de la Universidad del Litoral, un grupo de docentes está trabajando en una propuesta de Aprendizaje Cooperativo, estimulando y valorando habilidades sociales.En este trabajo, presentamos una experiencia de evaluación de habilidades de comunicación exhibidas por los alumnos en exámenes parciales orales en el cursado 2011. Los estudiantes, distribuídos en grupos de 4, recibieron un artículo de investigación en Ciencias Veterinarias, que incluía modelos matemáticos sencillos que ellos debían analizar y explicar. Para la ponderación de las competencias orales se emplearon grillas ad hoc, con consignas relacionadas con tono de voz, mirar al interlocutor a la cara, buen manejo del lenguaje oral y corporal, entre otros ítems.Los resultados mostraron que los alumnos presentan dificultades para expresar verbalmente sus conocimientos, escaso vocabulario, inseguridad y poca elocuencia. Esta instancia de integración de competencias orales y tareas asociadas a las motivaciones de los alumnos fue valorada como positiva por ellos, aún cuando los resultados no hayan sido tan satisfactorios.La propuesta intenta ofrecer un espacio donde sea posible corregir competencias comunicativas no asertivas como método para incluir otras variables a la evaluación tradicional de contenidos y procedimientos

NON-CANONICAL NOTCH SIGNALING IN T-ALL: A PHOSPHO-FLOW CYTOMETRY STUDY

Introduction. Deregulated Notch1 signaling has a fundamental role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL), in which the majority of human and murine tumors have acquired acti- vating mutations that lead to aberrant increases in Notch1 signaling. NOTCH1 encodes a transmembrane receptor acting as a ligand-acti- vated transcription factor and playing an important role in cell differ- entiation, proliferation, and apoptosis. Notch1 signaling initiates when the ligand, from either the Jagged or Delta families, binds to the receptor and induces successive proteolytic cleavages, resulting in the release and nuclear translocation of the Notch1 intra-cellular domain (NICD). In the nucleus, NICD assembles a transcriptional complex, leading to de-repression/activation of specific target genes. Besides this “canonical” signaling pathway involving ligand-induced cleavage of Notch for transcriptional regulation, a ligand- or transcription-inde- pendent (non-canonical) function of Notch has also been reported in various systems across species. However, in most cases, the key medi- ators of non-canonical Notch signals are unclear, and the proposed mechanisms appear to vary with context. In T-ALL, Notch non-canon- ical signals and their possible cytoplasmic mediators have been not investigated so far. Methods. To study the non-canonical Notch signal- ing pathway in T-ALL, we used multi-parametric phospho-flow cytometry to simultaneously determine protein expression and pro- tein post-translational modifications (i.e. phosphorylation) at a single cell level in T-ALL cell lines stimulated by the Notch1 ligand Jagged1. Then, protein expression of specific Notch target genes, as readout of Notch1 signaling activation, has been analyzed at slower time points whilst phosphorylation of signaling proteins, which are crucial for T- ALL pathogenesis, has been measured at rapid time points, to identi- fy possible cytoplasmic mediators of the non-canonical Notch1 signaling. Results. We showed that, besides the expression of specific Notch target proteins, Notch1 activation induced the rapid phospho- rylation of cytoplasmic proteins, namely STAT3, Akt, and Rb. Moreover, Notch1 activation evoked heterogeneous signaling profiles across different cell lines, which recapitulate ontogenetic stages in T- ALL. Conclusions. This study showed that “non canonical” cytoplasmic signals are induced in T-ALL in addition to slower transcriptional responses traditionally attributed to Notch activation. In addition, multi-parametric phospho-flow cytometry enables to distinguish Notch signaling network profiles that are associated with the T-ALL ontogeny stages. Identifying cytoplasmic mediators of the Notch non- canonical pathway as biologically relevant signaling hubs may repre- sent new challenges for anti-Notch1 therapy in T-ALL

Competencias sociales en la formación universitaria: las voces de sus actores

Las competencias sociales constituyen una herramienta básica en las relaciones interpersonales para alcanzar un grado óptimo de bienestar y ajuste social. Estas habilidades deberían requerirse en todos los espacios educativos y más en la Universidad, en donde se modelan los futuros profesionales quienes deben estar capacitados para comunicarse eficazmente, coordinar equipos, resolver conflictos interpersonales, etc.En la Facultad de Medicina Veterinaria de la UNL desarrollamos una investigación en la que intentamos poner en debate estas competencias. Inscribimos este proyecto desde el paradigma interpretativo, bajo un diseño mixto en el que, inicialmente describimos la situación desde la voz de sus actores (docentes, alumnos, empleadores) para luego hacer un abordaje cualitativo en el que tratamos de comprender la realidad circundante en su carácter específico. El diseño está estructurado en etapas que produjeron información que refinó las ideas previas, aportando nuevas posibles miradas.Establecimos como hipótesis que mejorar las competencias sociales puede mejorar la formación e inserción laboral de los egresados y que pueden fortalecerse desde las propuestas pedagógicas. Se trata de un diseño longitudinal, la unidad de observación es la Facultad de Veterinaria y la unidad de análisis los alumnos de dicha carrera.Los primeros resultados delimitaron el concepto de competencias sociales emergentes del compromiso educativo; encuestas a empleadores permitieron conocer sus expectativas al respecto; entrevistas personales y escalas de autopercepción a docentes y alumnos reflejan las competencias sociales reales y deseadas del escenario educativo. Su contraste con las aspiraciones del mercado laboral abre interrogantes, interpela al diseño curricular y sus estrategias de formación

The TNF-Family Cytokine TL1A/Death Receptor 3 System Reduces Metabolic Activity in Chronic Lymphocytic Leukemia B Cells

Tumor necrosis factor (TNF)-like cytokine 1A (TL1A) is a member of the TNF superfamily, expressed on dendritic cells, macrophages, lymphocytes, and endothelial cells. It is the only described ligand for death receptor 3 (DR3), a death-domain containing receptor of the TNF-receptor superfamily, mainly expressed on lymphocytes, natural killer (NK) cells, and NK-T cells. TL1A\u2013DR3 interaction results in co-stimulatory signaling for activated T cells, leading to amplification of inflammation and immune responses, correlated with greater pathogenicity in diverse autoimmune diseases. In contrast, in activated B cells the TL1A/DR3 system exerts inhibitory effect on cell proliferation, suggesting that TL1A may also have modulatory and homeostatic functions on B-cell expansion. Chronic lymphocytic leukemia (CLL) is the leukemia with the highest incidence among adults in Western countries. It is well documented that several elements within the tumor microenvironment, including antigens, cytokines, adhesion molecules, and surface receptors, play a fundamental role in supporting the growth of CLL. In contrast, little is known on regulatory mechanisms of CLL growth. In this study, we have investigated the possible regulatory role of the TL1A/DR3 system in B cells from CLL patients. CLL patients from the Hematology Unit at the University Hospital of Verona (Italy) were included in this study (n=37). Disease characteristics and demographic variables were collected on all patients. Purified B cells were obtained by negative selection. DR3 expression was measured on peripheral blood B cells by flow cytometry and western blot at baseline and following B cell receptor (BCR) stimulation with anti-human IgM. DR3 expression was confirmed on lymph-node CLL specimens by immunofluorescence. Metabolic activity of CLL B cells was analyzed by MTT assay. Apoptosis was analyzed by Annexin V assay. TL1A serum levels in CLL patients were measured by ELISA. Baseline analysis in vitro showed that DR3 was expressed at low levels in CLL B cells. Cell activation through stimulation of the BCR induced a significant increase of DR3 expression in a fraction of CLL B cells (p<0.001). Higher levels of DR3 expression were associated with early-stage (Rai 0) disease (p=0.019). The relevance of these findings was confirmed by immuofluorescence analysis of B-CLL lymph-node specimens showing that DR3 was expressed at high levels in some CLL B cells in vivo. Treatment of purified CLL B cells with exogenous recombinant TL1A in vitro, in the presence of BCR stimulation, induced a decreased metabolic activity in 3/8 B-CLL cell samples (37.5%). No change in CLL metabolic activity was observed following treatment with TL1A alone, in the absence of BCR stimulation. Treatment of B-CLL samples with TL1A, either in the presence or absence of BCR stimulation, induced no changes in cell viability, thus ruling out that decreased metabolic activity was due to reduced survival. A soluble form of TL1A was detected in the sera of CLL patients and higher serum levels of TL1A were significantly associated with early-stage (Rai 0) disease (p=0.023) and absence of CD38 expressions (p=0.035). In summary, this study shows that B-CLL metabolic activity can be reduced through the activity of the TL1A/DR3 system, in the presence of the BCR stimulation. Furthermore, TL1A and DR3 levels are higher in patients with early-stage disease. Taken together, these findings suggest that the TL1A/DR3 system in vivo, in the presence of antigen stimulation, may modulate leukemic cell metabolism in early-stage CLL, thus influencing the clinical course of disease

REDOX SIGNALING HYPERSENSITIVITY DISTINGUISHES CHRONIC LYMPHOCYTIC LEUKEMIA PATIENTS WITH FAVORABLE PROGNOSIS

Background. Chronic lymphocytic leukemia (CLL) patients exhibit a variable clinical course, with some patients having indolent disease and others experiencing a more accelerated course, treatment resistance and dismal outcome. The B-cell receptor (BCR) signaling is a key determinant of heterogeneous clinical behavior of CLL and is a target for therapeutic interventions. Endogenously produced H2O2 is thought to fine tune the level of BCR signaling by reversibly inhibiting phosphatases. However, relatively little is known about how CLL cells sense and respond to such redox cues. Aims. In this study, we used phospho-specific flow cytometry to compare BCR signaling responses to H2O2 in prognostic groups of CLL patients. Methods. The phosphorylation levels of five proteins downstream of the BCR signaling, namely SYK, NF-\u3baB p65, ERK1/2, p38 and JNK, were analyzed at the single-cell level in 26 CLL cell samples using phospho-specific flow cytometry. Protein phosphorylation was measured in the basal condition and following stimulation with H2O2. Circulating B cells from healthy individuals were analyzed as controls. The two-sample Wilcoxon\u2019s rank sum test was used to compare protein phosphorylation in groups of patients. Time to first treatment (TTFT) was calculated from the date of diagnosis to the date of initial therapy. TTFT curves estimated using the Kaplan- Meier method for the respective groups of patients were compared using the log-rank test. Results. In CLL cells, stimulation with H2O2 induced a statistically significant increase in phosphorylation of all analyzed signaling proteins with the exception of SYK. Moreover, the extents of responses to H2O2 were significantly higher in CLL than normal B cells for all signaling proteins but SYK. Comparison of H2O2 signaling response in prognostic groups of patients defined by IGHV mutational status, CD38 or ZAP-70 expression, showed that median phosphorylation response of ERK1/2 to H2O2 was significantly higher in the patient subset defined by the mutated IGHV status (M-CLL) (P=0.031). No significant correlations were observed between H2O2 responsiveness of BCR signaling proteins and ZAP-70 or CD38 expression. Kaplan-Meier curves showed statistically significant slower progression (longer time to first treatment, TTFT) in patients with higher p-ERK1/2 and p-NF-\uf06bB p65 responses to H2O2, indicating that lower responsiveness of these signaling proteins to H2O2 correlated with more rapid progression [median TTFT was 41.6 and 115 months for patients with lower and higher NK-\u3baB p65 responsiveness to H2O2, respectively (log-rank test P=0.0011); median TTFT was 38.7 and 117.0 months for patients with lower and higher ERK1/2 responsiveness to H2O2, respectively (log-rank test P=0.0008)] (Figure 1). Interestingly, the ability of H2O2 responsiveness signaling to define prognostic groups is comparable to that of IGHV mutational status (log-rank test P=0.0003). Conclusions. This study reveals that a novel H2O2 signaling response distinguishes a prognostic group of CLL patients with favorable prognosis. Specifically, higher H2O2 responsiveness of ERK1/2 or NF-\u3baB is predictive of longer TTFT, thus highlighting ERK and NF-\u3baB as biologically and clinically relevant signaling nodes in CLL

EXPRESSION AND FUNCTIONAL ACTIVITY OF THE TNFR-SUPERFAMILY MEMBER DEATH RECEPTOR 3 IN CHRONIC LYMPHOCYTIC LEUKEMIA B CELLS ACTIVATED BY THE BCR

Background: Growing evidences suggest a dynamic balance of B-cell chron- ic lymphocytic leukemia (B-CLL) cells between the blood and lymphoid tissues, which represent permissive niches for cell proliferation and survival. Within lymphoid tissue sites, molecules of the tumor necrosis factor (TNF) superfam- ily have been shown to play a supportive role and contribute to the pathogen- esis of B-CLL. Thereby, investigating expression and functions of novel TNFR- superfamily members in B-CLL would allow us to gain deeper insights into molecular crosstalk within leukemic microenvironments. Death receptor (DR) 3 is a TNFR-superfamily member expressed in lymphocyte-enriched tissues that binds to the TNF-like ligand 1A (TL1A), a TNF superfamily member. The TL1A/DR3 axis is implicated in regulatory mechanisms of adaptive immune response under physiological and pathological settings. Further evidence for the implication of TL1A in regulatory mechanisms arises from our recent data show- ing an inhibitory function of TL1A on B-cell proliferation. In leukemia cells, DR3 expression and functions have not been explored so far. CLL patients and to explore the possible role of TL1A/DR3 axis in the disease. Methods: B cells were purified from PBMC of 37 B-CLL patients by negative selection with magnetic beads. DR3 surface expression was measured by flow cytometry at baseline and following stimulation with F(ab’)2 anti-human IgM con- jugated to latex microspheres. DR3 expression was confirmed by western blot and immunofluorescence analysis on B-CLL lymph nodes. DR3 function was studied by MTT assay and Annexin V assay. TL1A serum levels were measured by ELISA. Results: Under basal conditions CLL B cells in vitro expressed low levels of DR3. Stimulation of the B cell receptor (BCR) with anti-IgM antibodies induced a sta- tistically significant increase of DR3 expression in CLL B cells (p<0.001). Induced DR3 expression showed great variability amongst B-CLL cells (variance (σ2)=6.38). Flow cytometry data were confirmed by Western blot analysis. The relevance of these findings was further confirmed by immuofluorescence analy- sis of B-CLL lymph-node specimens showing that in vivo high levels of DR3 were expressed by a number of B-CLL cells. To assess whether the anti-IgM-induced DR3 molecule was functionally active in CLL B cells, we examined the ability of DR3 to modulate their metabolic activity. Stimulation of DR3 with TL1A in the presence of BCR engagement showed that TL1A induced an equal or greater than 25% decrease of metabolic activity in 37.5% of B-CLL cell samples. In these samples the modulation is not due to reduced survival, as assessed by Annexin V assay. No change in metabolic activity was observed following TL1A treatment, in the absence of anti-IgM. Higher levels of DR3 expression were significantly associated with early-stage (Rai 0) disease (p=0.019) and higher serum levels of TL1A were significantly associated with early-stage (Rai 0) disease (p=0.023) and absence of CD38 expressions (p=0.035). CLL cells activated by the BCR stimulation express DR3 and TL1A reduces meta- bolic activity in some B-CLL cells. Herein, our data show a novel regulatory role for TL1A that, in the presence of antigen stimulation, may modulate leukemic cell metabolism through DR3 in early-stage B-CLL and suggest that homeostatic functions of TL1A may influence the clinical course of B-CLL disease

Expression and function of the TL1A/DR3 axis in chronic lymphocytic leukemia

TNF-like ligand 1A (TL1A) and its unique receptor death receptor 3 (DR3) acts as broad T-cell costimulator involved in regulatory mechanisms of adaptive immune response under physiological and pathological settings. Moreover, we have recently shown that TL1A negatively regulates B-cell proliferation. Despite increasing interest on the TL1A/DR3-axis functions, very little is known on its expression and role in leukemia. In this study, we investigated the expression and function of TL1A/DR3 axis in chronic lymphocytic leukemia (CLL). DR3 was differentially expressed in activated CLL cells and predominantly detected in patients with early clinical stage disease. Soluble TL1A has been revealed in the sera of CLL patients where higher TL1A levels were associated with early stage disease. T cells, monocytes and leukemic B cells have been identified as major sources of TL1A in CLL. The relevance of these findings has been sustained by functional data showing that exogenous TL1A reduces CLL proliferation induced by stimulation of the B cell receptor. Overall, these data document the expression of the TL1A/DR3 axis in early-stage CLL. They also identify a novel function for TL1A as a negative regulator of leukemic cell proliferation that may influence the CLL physiopathology and clinical outcome at an early-stage disease