La relación profesor-alumno en la educación secundaria: una revisión bibliográfica.

La relación profesor-alumno ha sido un constructo que se ha venido estudiando los últimos años debido a los beneficios que reporta tanto para el alumnado como para el profesorado. El objetivo del presente trabajo es hacer una revisión bibliográfica sobre las publicaciones recientes que abordan el tema de la relación profesor-alumno en la educación secundaria, para discernir las variables relacionadas más importantes con objeto de potenciar esta relación en la práctica docente. Tras la realización de una búsqueda sistemática, se obtuvo un total de siete publicaciones que cumplieron los criterios de inclusión. Si bien, hay que tener en cuenta que la falta de bibliografía enfocada en este tema ha dificultado la generalización y comparación de resultados, se considera que el vínculo afectivo es el eje central de la relación profesor-alumno y que es necesario ampliar el campo de investigación al respecto para dotar al profesorado de estrategias concretas para mejorar la relación con sus estudiantes.ABSTRACT. The teacher-student relationship is a construct that has been studied in recent years due to the benefits it brings to students and teachers. The aim of this project is to carry out a bibliographic review on recent publications that investigate teacher-student relationship in secondary education, in order to discern the most important related variables with a view to improve this relationship in teaching practice. After conducting a systematic review, we were able to find a total of seven publications that agreed the inclusion criteria. Although it must be taken into account that the lack of bibliography related to this topic has made it difficult to generalize and compare results, we have reached the conclusion that the affective bond is the central axis of the teacher-student relationship and it is necessary to expand the field of 5 research in this regard to provide teachers with specific strategies to improve the relationship with their students

Intolerancia a la incertidumbre, ansiedad y depresión en adolescentes: el papel mediador de la preocupación y la rumiación.

Máster Universitario en Psicología General Sanitaria Por la UllEl objetivo de este trabajo es conocer si los estilos rumiativos y la preocupación influyen como variables mediadoras en la relación entre la intolerancia a la incertidumbre y la existencia de síntomas ansiosos y depresivos. Para ello, se ha realizado un análisis mediacional por medio del PROCESS (Hayes, 2012; Hayes y Rockwood, 2017) del SPSS. Esta posible mediación se ha corroborado utilizando tanto el modelo directo, como el inverso (Hayes, 2012). La muestra ha estado formada por 303 adolescentes, de los que el 56,4% eran chicas y el 43,6% chicos. Tienen un rango de edad entre los 12 y los 17 años, siendo la media de 15.12, mientras que la moda de edad se sitúa en los 16 años. Los resultados han confirmado la existencia de un efecto mediador entre las variables propuestas, aunque obteniendo unos valores del efecto poco potente.The main objective of this work is to explore if ruminative styles and worry are mediating variables in the relationship between intolerance of uncertainty and the existence of anxious and depressive symptoms in teenagers. A mediational analysis has been carried out through PROCESS (Hayes, 2012; Hayes and Rockwood, 2017) of the SPSS. This possible mediation has been examinated using the direct and inverse model. A sample of 303 adolescents was used, in which 56.4% were girls and 43.6% boys. It has an age range between 12 and 17 years, the average has been 15.12, while the trend was 16 years. The results have confirmed the existence of a mediating effect between the proposed variables, although obtaining values of the weak effect.The main objective of this work is to explore if ruminative styles and worry are mediating variables in the relationship between intolerance of uncertainty and the existence of anxious and depressive symptoms in teenagers. A mediational analysis has been carried out through PROCESS (Hayes, 2012; Hayes and Rockwood, 2017) of the SPSS. This possible mediation has been examinated using the direct and inverse model. A sample of 303 adolescents was used, in which 56.4% were girls and 43.6% boys. It has an age range between 12 and 17 years, the average has been 15.12, while the trend was 16 years. The results have confirmed the existence of a mediating effect between the proposed variables, although obtaining values of the weak effect

Inflammation and metabolic dysregulation in diabetic cardiomyopathy

Podeu consultar el llibre complet a: http://hdl.handle.net/2445/67430Diabetic cardiomyopathy is characterized by structural and functional alterations in the heart muscle of people with diabetes that finally lead to heart failure. Metabolic disturbances characterized by increased lipid oxidation, intramyocardial triglyceride accumulation and reduced glucose utilization have all been involved in the pathogenesis of diabetic cardiomyopathy. On the other hand, evidences arisen in the recent years point to a potential link between chronic low-grade inflammation in the heart and metabolic dysregulation. Interestingly, the progression of heart failure and cardiac hypertrophy usually entails the activation of pro-inflammatory pathways. Therefore, in this chapter we summarize novel insights into the crosstalk between inflammatory processes and metabolic dysregulation in the failing heart during diabetes

Peroxisome Proliferator-Activated Receptor β/δ (PPAR β/δ) as a Potential Therapeutic Target for Dyslipidemia

Dyslipidemia is a powerful predictor of cardiovascular disease in patients at high risk (Turner et al., 1998), such as type 2 diabetic patients. Lowering of LDL-C is the prime target for treatment (2002), but even with intensification of statin therapy, a substantial residual cardiovascular risk remains (Barter et al., 2007; Miller et al., 2008; Fruchart et al., 2008; Shepherd et al., 2006). This may partly be due to atherogenic dyslipidemia. This term is commonly used to describe a condition of abnormally elevated plasma triglycerides and low high-density lipoprotein cholesterol (HDL-C), irrespective of the levels of LDL-C (Grundy, 1995). In addition to these key components, increased levels of small, dense LDL-C particles are also present, which in conjunction with the former components conform the also called “lipid triad” (Shepherd et al., 2005). Other abnormalities include accumulation in plasma of triglyceride-rich lipoproteins (TLRs), including chylomicron and very-low-density lipoprotein (VLDL) remnants. This is reflected by elevated plasma concentrations of non- HDL-C and apolipoprotein B-100 (apoB). Postprandially, there is also accumulation in plasma of TLRs and their remnants, as well as qualitative alterations in LDL and HDL particles. Thus, hypertriglyceridemia is associated with a wide spectrum of atherogenic lipoproteins not measured routinely (Taskinen, 2003). The presence of this lipid plasma profile with high triglyceride and low HDL-C levels have been shown to increase the risk of cardiovascular events independent of conventional risk factors (Bansal et al., 2007; Barter et al., 2007; deGoma et al., 2008). In fact, guidelines recommend modifying high triglyceride and low HDL-C as secondary therapeutic targets to provide additional vascular protection (2002). The presence of atherogenic dyslipidemia is seen in almost all patients with triglycerides > 2.2 mmol/l and HDL-C < 1.0 mmol/l, virtually all of whom have type 2 diabetes or abdominal obesity and insulin resistance (Taskinen, 2003)..

Design and Synthesis of AMPK Activators and GDF15 Inducers

Targeting growth differentiation factor 15 (GDF15) is a recent strategy for the treatment of obesity and type 2 diabetes mellitus (T2DM). Here, we designed, synthesized, and pharmacologically evaluated in vitro a novel series of AMPK activators to upregulate GDF15 levels. These compounds were structurally based on the (1-dibenzylamino-3-phenoxy)propan-2-ol structure of the orphan ubiquitin E3 ligase subunit protein Fbxo48 inhibitor, BC1618. This molecule showed a better potency than metformin, increasing GDF15 mRNA levels in human Huh-7 hepatic cells. Based on BC1618, structural modifications have been performed to create a collection of diversely substituted new molecules. Of the thirty-five new compounds evaluated, compound 21 showed a higher increase in GDF15 mRNA levels compared with BC1618. Metformin, BC1618, and compound 21 increased phosphorylated AMPK, but only 21 increased GDF15 protein levels. Overall, these findings indicate that 21 has a unique capacity to increase GDF15 protein levels in human hepatic cells compared with metformin and BC1618

PPARβ/δ: A Key Therapeutic Target in Metabolic Disorders

Research in recent years on peroxisome proliferator-activated receptor (PPAR)β/δ indicates that it plays a key role in the maintenance of energy homeostasis, both at the cellular level and within the organism as a whole. PPARβ/δ activation might help prevent the development of metabolic disorders, including obesity, dyslipidaemia, type 2 diabetes mellitus and non-alcoholic fatty liver disease. This review highlights research findings on the PPARβ/δ regulation of energy metabolism and the development of diseases related to altered cellular and body metabolism. It also describes the potential of the pharmacological activation of PPARβ/δ as a treatment for human metabolic disorder

SIRT3 deficiency exacerbates fatty liver by attenuating the HIF1α-LIPIN 1 pathway and increasing CD36 through Nrf2

Background: Deficiency of mitochondrial sirtuin 3 (SIRT3), a NAD+ -dependent protein deacetylase that maintains redox status and lipid homeostasis, contributes to hepatic steatosis. In this study, we investigated additional mechanisms that might play a role in aggravating hepatic steatosis in Sirt3-deficient mice fed a high-fat diet (HFD). Methods: Studies were conducted in wild-type (WT) and Sirt3−/− mice fed a standard diet or a HFD and in SIRT3- knockdown human Huh-7 hepatoma cells. Results: Sirt3−/− mice fed a HFD presented exacerbated hepatic steatosis that was accompanied by decreased expression and DNA-binding activity of peroxisome proliferator-activated receptor (PPAR) α and of several of its target genes involved in fatty acid oxidation, compared to WT mice fed the HFD. Interestingly, Sirt3 deficiency in liver and its knockdown in Huh-7 cells resulted in upregulation of the nuclear levels of LIPIN1, a PPARα co-activator, and of the protein that controls its levels and localization, hypoxia-inducible factor 1α (HIF-1α). These changes were prevented by lipid exposure through a mechanism that might involve a decrease in succinate levels. Finally, Sirt3−/− mice fed the HFD showed increased levels of some proteins involved in lipid uptake, such as CD36 and the VLDL receptor. The upregulation in CD36 was confirmed in Huh-7 cells treated with a SIRT3 inhibitor or transfected with SIRT3 siRNA and incubated with palmitate, an effect that was prevented by the Nrf2 inhibitor ML385. Conclusion: These findings demonstrate new mechanisms by which Sirt3 deficiency contributes to hepatic steatosi

State of the art on toxicological mechanisms of metal and metal oxide nanoparticles and strategies to reduce toxicological risks

Metal nanoparticles have been extensively investigated for different types of pharmaceutical applications. However, their use has raised some concerns about their toxicity involving the increase of reactive oxygen species causing cellular apoptosis. Therefore, in this review we summarize the most relevant toxicity mechanisms of gold, silver, copper and copper oxide nanoparticles as well as production methods of metal nanoparticles. Parameters involved in their toxicity such as size, surface charge and concentration are also highlighted. Moreover, a critical revision of the literature about the strategies used to reduce the toxicity of this type of nanoparticles is carried out throughout the review. Additionally, surface modifications using different coating strategies, nanoparticles targeting and morphology modifications are deeply explained.This work was funded by the Portuguese Science and Technology Foundation (FCT) from the Ministry of Science and Technology (MCTES), European Social Fund (FSE) of EU, through the project UIDB/04469/2020 (CEB strategic fund), co-funded by European Funds (PRODER/COMPETE) and FEDER, under the Partnership Agreement PT2020.info:eu-repo/semantics/publishedVersio

CHOP upregulation and dysregulation of the mature form of the SNAT2 amino acid transporter in the placentas from small for gestational age newborns

[Background]: The placentas from newborns that are small for gestational age (SGA; birth weight < -2 SD for gestational age) may display multiple pathological characteristics. A key determinant of fetal growth and, therefore, birth weight is placental amino acid transport, which is under the control of the serine/threonine kinase mechanistic target of rapamycin (mTOR). The effects of endoplasmic reticulum (ER) stress on the mTOR pathway and the levels of amino acid transporters are not well established. [Methods]: Placentas from SGA and appropriate for gestational age (AGA) newborns and the human placental BeWo cell line exposed to the ER stressor tunicamycin were used. [Results]: We detected a significant increase in the levels of C/EBP homologous protein (CHOP) in the placentas from SGA newborns compared with those from AGA newborns, while the levels of other ER stress markers were barely affected. In addition, placental mTOR Complex 1 (mTORC1) activity and the levels of the mature form of the amino acid transporter sodium-coupled neutral amino acid transporter 2 (SNAT2) were also reduced in the SGA group. Interestingly, CHOP has been reported to upregulate growth arrest and DNA damage-inducible protein 34 (GADD34), which in turn suppresses mTORC1 activity. The GADD34 inhibitor guanabenz attenuated the increase in CHOP protein levels and the reduction in mTORC1 activity caused by the ER stressor tunicamycin in the human placental cell line BeWo, but it did not recover mature SNAT2 protein levels, which might be reduced as a result of defective glycosylation. [Conclusions]: Collectively, these data reveal that GADD34A activity and glycosylation are key factors controlling mTORC1 signaling and mature SNAT2 levels in trophoblasts, respectively, and might contribute to the SGA condition.This study was partly supported by the grants RTI2018-093999-B-I00 and PID2021-122116OB-I00 (M.V.-C.) from MCIN/AEI/10.13039/501100011033 and “ERDF, A Way of Making Europe”. CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) is a Carlos III Health Institute project. Support was also received from the CERCA Programme/Generalitat de Catalunya

A positive feedback loop between AMPK and GDF15 promotes metformin antidiabetic effects

BACKGROUND AND AIMS: Metformin, the most prescribed drug for the treatment of type 2 diabetes mellitus, has been recently reported to promote weight loss by upregulating the anorectic cytokine growth differentiation factor 15 (GDF15). Since the antidiabetic effects of metformin are mostly mediated by the activation of AMPK, a key metabolic sensor in energy homeostasis, we examined whether the activation of this kinase by metformin was dependent on GDF15. METHODS: Cultured hepatocytes and myotubes, and wild-type and Gdf15(-/-) mice were utilized in a series of studies to investigate the involvement of GDF15 in the activation of AMPK by metformin. RESULTS: A low dose of metformin increased GDF15 levels without significantly reducing body weight or food intake, but it ameliorated glucose intolerance and activated AMPK in the liver and skeletal muscle of wild-type mice but not Gdf15(-/-) mice fed a high-fat diet. Cultured hepatocytes and myotubes treated with metformin showed AMPK-mediated increases in GDF15 levels independently of its central receptor GFRAL, while Gdf15 knockdown blunted the effect of metformin on AMPK activation, suggesting that AMPK is required for the metformin-mediated increase in GDF15, which in turn is needed to sustain the full activation of this kinase independently of the CNS. CONCLUSION: Overall, these findings uncover a novel mechanism through which GDF15 upregulation by metformin is involved in achieving and sustaining full AMPK activation by this drug independently of the CNS