Evaluación de metodologías didácticas en trabajos de fin de grado en titulaciones de Ciencias Experimentales

Mediante encuestas a estudiantes que se encuentran finalizando el Trabajo de Fin de Grado (TFG) y profesores que dirigen de los seis grados de la facultad de Ciencias (Biología, Ciencias del Mar, Geología, Matemáticas, Óptica y Optometría, Química) de la Universidad de Alicante, se han identificado los puntos de menor fortaleza de los TFGs independientemente para cada grado. A continuación, hemos comparado los resultados entre grados para ver el nivel de similitud entre ellos y la singularidad de cada uno de ellos. A partir de ahí, hemos identificado los posibles factores que configuran cada TFG con el fin de intentar entender su singularidad en cada caso. Esta información es importante para ayudarnos a comprender cómo se podrían fortalecer posibles carencias en TFGs específicos. Con esta información y en base a la experiencia previa, proponemos medidas que permitan favorecer la implementación y desarrollo de los TFGs. Con estas propuestas se espera mejorar la eficiencia de los TFGs y conseguir un mayor nivel de satisfacción y el rendimiento en esta asignatura común en todos los grados

Análisis de los Trabajos de Fin de Grado desde la visión docente

El Trabajo Fin de Grado (TFG) en los grados de la Facultad de Ciencias, constituye una asignatura con importantes competencias transversales que representa la fase final del plan de estudios, y supone la realización por parte del estudiante de un proyecto, memoria o estudio bajo la supervisión de un tutor o tutora. En este trabajo se realiza un estudio general de los TFGs y la utilización del UA-project, desde la visión del profesorado. Para poder optimizar el desarrollo de los TFGs, en este trabajo se realizó un análisis interno mediante un cuestionario. Para dar mayor amplitud y proyección a la propuesta se han enviado los cuestionarios a profesores de todos los grados de la Facultad de Ciencias: Biología, Ciencias del Mar, Química, Geología, Matemáticas y Óptica y Optometría. Estos cuestionarios reflejan la experiencia docente obtenida en los últimos años en la tutorización de los TFGs, para así poder obtener conclusiones e ideas de mejora para su posterior aplicación

Adaptación de los TFGs de Ciencias al Espacio Europeo de Educación Superior: valoración del alumnado

Este estudio tiene el objetivo de obtener una percepción desde el punto de vista del alumnado del Trabajo de Fin de Grado (TFG). Para ello, se realizaron encuestas a estudiantes de grado que están finalizando el (TFG) en la facultad de Ciencias (Biología, Ciencias del Mar, Geología, Matemáticas, Óptica y Optometría, y Química) de la Universidad de Alicante. En un principio, se analizaron para cada grado de forma independiente con el propósito de tener una visión global de la percepción de los alumnos para cada grado. A continuación, se contrastaron los resultados obtenidos entre los grados para buscar posibles similitudes entre ellos y entender las singularidades de cada uno. Mediante este estudio podemos conocer la opinión sobre TFG desde el punto de vista del alumnado. Dichos resultados pueden sentar las bases para enriquecer y optimizar el desarrollo de los TFGs con el fin de favorecer su capacidad formativa al ser una asignatura obligatoria común en todos los grados

Innovación docente en trabajos de fin de grado en Ciencias del Mar y grados afines

El Trabajo Fin de Grado (TFG) es una asignatura con unas características especiales y de nueva instauración en la mayoría de los grados de las universidades españolas. El objetivo de este estudio fue analizar la implementación y desarrollo del TFG con el fin de evaluar posibles carencias y, en su caso, poner medidas para corregirlas. Para este fin, se realizaron encuestas específicas tanto a alumnos que estaban en ese momento finalizando el TFG como a profesores que estaban tutorizando o habían tutorizado TFGs. En base a los resultados obtenidos creemos que se debería trabajar más en la orientación e información a los alumnos, de los distintos aspectos del TFG mediante charlas informativas. La dedicación docente derivada de la tutorización de los TFGs debería tenerse en cuenta en el cómputo de horas lectivas del POD. Adicionalmente, el tutor de un TFG debería formar parte en la evaluación de dicho TFG. La normativa de los TFGs debería ser menos rígida para favorecer los trámites administrativos. Especialmente importante sería dotar a la aplicación UA-project de una mayor flexibilidad

Inhibition of Gsk3b Reduces Nfkb1 Signaling and Rescues Synaptic Activity to Improve the Rett Syndrome Phenotype in Mecp2-Knockout Mice

Rett syndrome (RTT) is the second leading cause of mental impairment in girls and is currently untreatable. RTT is caused, in more than 95% of cases, by loss-of-function mutations in the methyl CpG- binding protein 2 gene (MeCP2). We propose here a molecular target involved in RTT: the glycogen synthase kinase-3b (Gsk3b) pathway. Gsk3b activity is deregulated in Mecp2-knockout (KO) mice models, and SB216763, a specific inhibitor, is able to alleviate the clinical symptoms with consequences at the molecular and cellular levels. In vivo, inhibition of Gsk3b prolongs the lifespan of Mecp2-KO mice and reduces motor deficits. At the molecular level, SB216763 rescues dendritic networks and spine density, while inducing changes in the properties of excitatory synapses. Gsk3b inhibition can also decrease the nuclear activity of the Nfkb1 pathway and neuroinflammation. Altogether, our findings indicate that Mecp2 deficiency in the RTT mouse model is partially rescued following treatment with SB216763

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Summary Background Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. Methods We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung’s disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. Findings We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung’s disease) from 264 hospitals (89 in high-income countries, 166 in middleincome countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in lowincome countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. Interpretation Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between lowincome, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Inhibition of Gsk3b Reduces Nfkb1 Signaling and Rescues Synaptic Activity to Improve the Rett Syndrome Phenotype in Mecp2-Knockout Mice

Summary: Rett syndrome (RTT) is the second leading cause of mental impairment in girls and is currently untreatable. RTT is caused, in more than 95% of cases, by loss-of-function mutations in the methyl CpG-binding protein 2 gene (MeCP2). We propose here a molecular target involved in RTT: the glycogen synthase kinase-3b (Gsk3b) pathway. Gsk3b activity is deregulated in Mecp2-knockout (KO) mice models, and SB216763, a specific inhibitor, is able to alleviate the clinical symptoms with consequences at the molecular and cellular levels. In vivo, inhibition of Gsk3b prolongs the lifespan of Mecp2-KO mice and reduces motor deficits. At the molecular level, SB216763 rescues dendritic networks and spine density, while inducing changes in the properties of excitatory synapses. Gsk3b inhibition can also decrease the nuclear activity of the Nfkb1 pathway and neuroinflammation. Altogether, our findings indicate that Mecp2 deficiency in the RTT mouse model is partially rescued following treatment with SB216763. : Rett syndrome (RTT) is a severe neurodevelopmental disorder characterized by loss-of-function mutations in the MeCP2 gene. Jorge-Torres et al. show that mice models of RTT display hyperactivation of Gsk3b kinase and neuroinflammation. Inhibition of the Gsk3b pathway partially rescues the phenotype and affects neuronal morphology and synaptic activity. Keywords: Rett syndrome, Gsk3b, Nfkb1, neurons, mice models, SB216763, neuroinflammation, Mecp

PLCG1 mutations in cutaneous T-cell lymphomas

Cutaneous T-cell lymphoma (CTCL) is a heterogeneous group of primary cutaneous T-cell lymphoproliferative processes, mainly composed of mycosis fungoides and Sezary syndrome, the aggressive forms of which lack an effective treatment. The molecular pathogenesis of CTCL is largely unknown, although neoplastic cells show increased signaling from T-cell receptors (TCRs). DNAs from 11 patients with CTCL, both normal and tumoral, were target-enriched and sequenced by massive parallel sequencing for a selection of 524 TCR-signaling-related genes. Identified variants were validated by capillary sequencing. Multiple mutations were found that affected several signaling pathways, such as TCRs, nuclear factor kappa B, or Janus kinase/signal transducer and activator of transcription, but PLCG1 was found to be mutated in 3 samples, 2 of which featured a redundant mutation (c.1034T&gt;C, S345F) in exon 11 that affects the PLCx protein catalytic domain. This mutation was further analyzed by quantitative polymerase chain reaction genotyping in a new cohort of 42 patients with CTCL, where it was found in 19% of samples. Immunohistochemical analysis for nuclear factor of activated T cells (NFAT) showed that PLCG1-mutated cases exhibited strong NFAT nuclear immunostaining. Functional studies demonstrated that PLCG1 mutants elicited increased downstream signaling toward NFAT activation, and inhibition of this pathway resulted in reduced CTCL cell proliferation and cell viability. Thus, increased proliferative and survival mechanisms in CTCL may partially depend on the acquisition of somatic mutations in PLCG1 and other genes that are essential for normal T-cell differentiation