Familias monoparentales usuarias de los Puntos de Encuentro Familiar. El papel del/la Educador/a Social

Desde el pasado año 2012 el DECRETO 10/2012, de 22 de marzo, por el que se modifica el Decreto 11/2010, de 4 de marzo, por el que se regulan los Puntos de Encuentro Familiar en Castilla y León y su autorización de funcionamiento, establece que la figura del/la Educador/a Social formará parte del equipo técnico de los Puntos de Encuentro Familiar (en adelante PEF). Partiendo de esta nueva situación presumimos que la figura del/la Educador/a Social en los PEF precisa de formación continua que permita el desarrollo de la función profesional en este nuevo contexto de intervención. Para ello, en este Trabajo de Fin de Grado realizamos un análisis comparativo entre las competencias del Grado en Educación Social de la Universidad de Valladolid y las competencias implícitas en los Programas de Intervención en los Puntos de Encuentro Familiar con los que se da respuesta a las necesidades y demandas de las familias monoparentales en conflicto, usuarias de este recurso. El resultado de ese análisis se concreta en una propuesta de acción formativa que, junto con la experiencia adquirida en el contexto de trabajo, permita la especialización para el desempeño de la función del/la Educador/a Social en dicho contexto. A modo de síntesis se presentan los objetivos generales, las áreas de interés y los requisitos necesarios para el acceso a dicha formación.Grado en Educación Socia

Snail1 induces IL-17 expression to inhibit adipogenesis

44 p.-7 fig.-1 tab. Peláez-García, Alberto et al.Adipogenesis requires a differentiation program driven by multiple transcription factors, where PPARγ and C/EBPα play a central role. Recent findings indicate that Snail inhibits adipocyte differentiation in 3T3-L1 and murine mesenchymal stem cells (mMSC). An in-depth quantitative SILAC analysis of the nuclear fraction of Snail-induced alterations of 3T3-L1 cells was carried out. In total, 2251 overlapping proteins were simultaneously quantified in forward and reverse experiments. We observed 574 proteins deregulated by Snail1 using a fold-change ≥1.5, with 111 up- and 463 down-regulated proteins, respectively. Among other proteins, multiple transcription factors such as Trip4, OsmR, Nr2f6, Cbx6, and Prrx1 were down-regulated. Results were validated in 3T3-L1 cells and mMSC cells by Western blot and quantitative PCR. Knock-down experiments in 3T3-L1 cells demonstrated that only Nr2f6 (and Trip4 at minor extent) was required for adipocyte differentiation. Ectopic expression of Nr2f6 reversed the effects of Snail1 and promoted adipogenesis. Because Nr2f6 inhibits the expression of IL-17, we tested the effect of Snail on IL-17 expression. IL-17 and TNFα were among the most up-regulated pro-inflammatory cytokines in Snail-transfected 3T3-L1 and mMSC cells. Furthermore, the blocking of IL-17 activity in Snail-transfected cells promoted adipocyte differentiation, reverting Snail inhibition. In summary, Snail inhibits adipogenesis through a down-regulation of Nr2f6, which in turn facilitates the expression of IL-17, an anti-adipogenic cytokine. These results would support a novel and important role for Snail and Nr2f6 in obesity control.This research was supported by a grant to established research groups (AECC), grant BIO2012-31023 from the Ministry of Economy and Competitiveness, grant S2011/BMD-2344/ (Colomics2) from Comunidad de Madrid and ProteoRed-ISCIII support. Work at AGH’s lab was supported by a grant from the Ministry of Economy and Competitiveness (SAF2010-16089)Peer reviewe

VE-cadherin RGD motifs promote metastasis and constitute a potential therapeutic target in melanoma and breast cancers

13 p.-6 fig.We have investigated the role of vascular-endothelial (VE)-cadherin in melanoma and breast cancer metastasis. We found that VE-cadherin is expressed in highly aggressive melanoma and breast cancer cell lines. Remarkably, inactivation of VEcadherin triggered a significant loss of malignant traits (proliferation, adhesion, invasion and transendothelial migration) in melanoma and breast cancer cells. These effects, except transendothelial migration, were induced by the VE-cadherin RGD motifs. Co-immunoprecipitation experiments demonstrated an interaction between VE-cadherin and α2β1 integrin, with the RGD motifs found to directly affect β1 integrin activation. VE-cadherin-mediated integrin signaling occurred through specific activation of SRC, ERK and JNK, including AKT in melanoma. Knocking down VEcadherin suppressed lung colonization capacity of melanoma or breast cancer cells inoculated in mice, while pre-incubation with VE-cadherin RGD peptides promoted lung metastasis for both cancer types. Finally, an in silico study revealed the association of high VE-cadherin expression with poor survival in a subset of melanoma patients and breast cancer patients showing low CD34 expression. These findings support a general role for VE-cadherin and other RGD cadherins as critical regulators of lung and liver metastasis in multiple solid tumours. These results pave the way for cadherin-specific RGD targeted therapies to control disseminated metastasis in multiple cancers.BEP was an FPI fellow from Ministry of Economy and Competitiveness (MINECO). This research was supported by grants BIO2012-31023 and BIO2015-66849 from MINECO and PRB2 (IPT13/0001-ISCIII-SGEFI/FEDER) to JIC.Peer reviewe

¿Los estudios de prevalencia de zona básica de salud tienen sentido en medicina familiar y comunitaria? A propósito de un caso: la enfermedad pulmonar obstructiva crónica

ResumenObjetivoDeterminar la prevalencia de EPOC y tabaquismo en nuestra Zona Básica de Salud (ZBS) y su correlación con la prevalencia extrapolada y la morbilidad registrada. Conocer el perfil personal, familiar y social. Determinar la validez del test de función pulmonar.DiseñoEstudio de prevalencia.EmplazamientoZBS urbana.ParticipantesDocientas treinta y tres personas de 40 a 75años seleccionadas aleatoriamente.Mediciones principalesEdad, sexo, paquetes/año, espirometría, pulsioximetría, medicación, ingresos. Tests: Fagerström, Richmond, MOS, APGAR y función pulmonar.ResultadosEdad media: 53,7±7,6años; 57,9% mujeres. EPOC: morbilidad registrada 1,2% (0,5-3,9%). Prevalencia: 4,7% (1,5% mujeres, 9,2% hombres); prevalencia extrapolada: 10,2%. Tabaquismo: morbilidad registrada: 10,7% (1-19,4%); prevalencia: 18,5% (20% mujeres, 16,3% hombres); prevalencia extrapolada: 23,95%. Test de función pulmonar: cociente de probabilidad positivo: 3,18, y negativo: 0,1. Alta probabilidad de EPOC (59,5%) si >30paquetes/año. Los fumadores fuman como media 20,8paquetes/año. Dependencia física más alta en mujeres (36% versus 21,4%). Mayor probabilidad de deshabituación tabáquica en hombres (57,1% versus 44%). El 14,7% percibe disfunción familiar. El 6,9% tienen bajo apoyo social y el 9,1% en EPOC. El 70% de los pacientes EPOC nunca han ingresado. El 10% son polimedicados versus el 60% de los EPOC.ConclusionesLas prevalencias de EPOC y de tabaquismo (indicador de morbilidad evitable imputable a atención primaria) son sustancialmente inferiores a las prevalencias extrapoladas. El test de función pulmonar es válido. La variablidad interprofesional es elevada. Las mujeres fuman más, tienen más dependencia y menos motivación para el abandono. Su percepción familiar y social es peor. Estas investigaciones son fundamentales para la intervención comunitaria y la planificación operativa.AbstractObjectiveTo determine the prevalence of COPD and smoking in a Health District, to correlate real, registered, and extrapolated morbidity. To determine personal, family and social profiles. To determine the validity of the lung function questionnaire.DesignPrevalence study.LocationUrban District Health.ParticipantsRandom selection of 233 people aged 40-75years.Main measurementsAge, sex, pack/years, spirometry, pulse-oximetry, medication, income. Tests: Fagerström, Richmond, MOS, APGAR, and lung function.ResultsMean age was 53.7+7.6years, with 57.9% women. Registered morbidity for COPD 1.2% (0.5-3.9%). Prevalence 4.7% (1.5% female, 9.2% male), extrapolated prevalence: 10.2%. Registered morbidity for Smoking 10.7% (1-19.4%); prevalence: 18.5% (20% female, 16.3% male), extrapolated prevalence 23.95%. Lung function questionnaire: positive likelihood ratio 3.18; negative 0.1. High probability of COPD (59.5%) in >30 packs/year smokers. Smokers consume a mean of 20.8 packs/year. Women showed higher physical dependence (36% versus 21%). More probability of achieving successful smoking cessation in men (57.1% versus 44%). There was 14.7% perceived family dysfunction; 6.9% have a low global index of social support, and 9.1% in COPD subjects. More than two-thirds (70%) of COPD patients had never been hospitalized. There were 10% polymedicated patients compared to 60% in identified COPDs.ConclusionsPrevalence of COPD and smoking (indicator of avoidable morbidity attributable to primary care) are substantially lower than the reference data. The lung function questionnaire is valid. There was evidence of inter-professional variability. Women smoke more, are more dependent and are less motivated to quit. Their family and social perception is worse. These investigations are essentials for community intervention and operational planning

Caracterización del secretoma asociado a metástasis de cáncer colorrectal mediante SILAC utilizando el sistema celular KM12

Comunicaciones a congreso

Functional Proteomics Characterization of the Role of SPRYD7 in Colorectal Cancer Progression and Metastasis

SPRY domain-containing protein 7 (SPRYD7) is a barely known protein identified via spatial proteomics as being upregulated in highly metastatic-to-liver KM12SM colorectal cancer (CRC) cells in comparison to its isogenic poorly metastatic KM12C CRC cells. Here, we aimed to analyze SPRYD7’s role in CRC via functional proteomics. Through immunohistochemistry, the overexpression of SPRYD7 was observed to be associated with the poor survival of CRC patients and with an aggressive and metastatic phenotype. Stable SPRYD7 overexpression was performed in KM12C and SW480 poorly metastatic CRC cells and in their isogenic highly metastatic-to-liver-KM12SM-and-to-lymph-nodes SW620 CRC cells, respectively. Upon upregulation of SPRYD7, in vitro and in vivo functional assays confirmed a key role of SPRYD7 in the invasion and migration of CRC cells and in liver homing and tumor growth. Additionally, transient siRNA SPRYD7 silencing allowed us to confirm in vitro functional results. Furthermore, SPRYD7 was observed as an inductor of angiogenesis. In addition, the dysregulated SPRYD7-associated proteome and SPRYD7 interactors were elucidated via 10-plex TMT quantitative proteins, immunoproteomics, and bioinformatics. After WB validation, the biological pathways associated with the stable overexpression of SPRYD7 were visualized. In conclusion, it was demonstrated here that SPRYD7 is a novel protein associated with CRC progression and metastasis. Thus, SPRYD7 and its interactors might be of relevance in identifying novel therapeutic targets for advanced CRC

Preventive Gambling Programs for Adolescents and Young Adults: A Systematic Review

Gambling disorder in youth is an emerging public health problem, with adolescents and young adults constituting a vulnerable age group for the development of gambling-related problems. Although research has been conducted on the risk factors for gambling disorder, very few rigorous studies can be found on the efficacy of preventive interventions in young people. The aim of this study was to provide best practice recommendations for the prevention of disordered gambling in adolescents and young adults. We reviewed and synthesized the results of existing RCTs and quasi-experimental studies covering nonpharmacological prevention programs for gambling disorder in young adults and adolescents. We applied the PRISMA 2020 statement and guidelines to identify 1483 studies, of which 32 were included in the systematic review. All studies targeted the educational setting, i.e., high school and university students. Most studies followed a universal prevention strategy, that particularly targeted adolescents, and an indicated prevention strategy for university students. The reviewed gambling prevention programs generally showed good results in terms of reducing the frequency and severity of gambling, and also regarding cognitive variables, such as misconceptions, fallacies, knowledge, and attitudes towards gambling. Finally, we highlight the need to develop more comprehensive prevention programs that incorporate rigorous methodological and assessment procedures before they are widely implemented and disseminated

Are Reduced Levels of Coagulation Proteins Upon Admission Linked to COVID-19 Severity and Mortality?

Background: The link between coagulation system disorders and COVID-19 has not yet been fully elucidated. Aim: Evaluating the association of non-previously reported coagulation proteins with COVID-19 severity and mortality. Design: Cross-sectional study of 134 COVID-19 patients recruited at admission and classified according to the highest COVID-19 severity reached (asymptomatic/mild, moderate, or severe) and 16 healthy control individuals. Methods: Coagulation proteins levels (antithrombin, prothrombin, factor_XI, factor_XII, and factor_XIII) and CRP were measured in plasma by the ProcartaPlex Panel (Invitrogen) multiplex immunoassay upon diagnosis. Results: We found higher levels of antithrombin, prothrombin, factor XI, factor XII, and factor XIII in asymptomatic/mild and moderate COVID-19 patients compared to healthy individuals. Interestingly, decreased levels of antithrombin and factors XI, XII, and XIII were observed in those patients who eventually developed severe illness. Additionally, survival models showed us that patients with lower levels of these coagulation proteins had an increased risk of death. Conclusion: COVID-19 provokes early increments of some specific coagulation proteins in most patients. However, lower levels of these proteins at diagnosis might "paradoxically" imply a higher risk of progression to severe disease and COVID-19-related mortality.This study was supported by grants from Instituto de Salud Carlos III [ISCIII; Grant Number COV20/1144 (MPY224/20) to AF-R/MJ-S]. AF-R, MJ-S, and MR are Miguel Servet researchers supported and funded by ISCIII (Grant Numbers: CP14CIII/00010 to AF-R, CP17CIII/00007 to MJ-S, and CP19CIII/00002 to MR).S

An RGD motif present in cadherin 17 induces integrin activation and tumor growth

15 p.-9 fig.Little is known about the mechanism of integrin activation by cadherin 17 (CDH17). Here we observed the presence of a tri-peptide motif, RGD, in domain 6 of the human CDH17 sequence and other cadherins such as cadherin 5 and cadherin 6. The use of CDH17 RAD mutants demonstrated a considerable decrease of proliferation and adhesion in RKO and KM12SM colon cancer cells. Furthermore, RGD peptides inhibited the adhesion of both cell lines to recombinant CDH17 domain 6. The RGD motif added exogenously to the cells provoked a change in β1 integrin to an active, high-affinity conformation and an increase in focal adhesion kinase and ERK1/2 activation. In vivo experiments with Swiss nude mice demonstrated that cancer cells expressing the CDH17 RAD mutant showed a considerable delay in tumor growth and liver homing. CDH17 RGD effects were also active in pancreatic cancer cells. Our results suggest that α2β1 integrin interacts with two different ligands, collagen IV and CDH17, using two different binding sites. In summary, the RGD binding motif constitutes a switch for integrin pathway activation and shows a novel capacity of CDH17 as an integrin ligand. This motif could be targeted to avoid metastatic dissemination in tumors overexpressing CDH17 and other RGD-containing cadherins.This research was supported by grant BIO2012-31023 from the Spanish Ministry of Economy and Competitiveness, by a grant to established research groups (AECC), and by grant S2011/BMD-2344/ (Colomics2) from Comunidad de Madrid and ProteoRed-ISCIII.Peer reviewe