The spanish equality law and the gender balance in the evaluation committees: an opportunity for women’s promotion in higher education

Despite advances in gender policy and equality laws in the twenty-first century, women are still a minority in the full professor category in Europe. Some measures establish gender quotas to balance gatekeeper positions, which will supposedly pave the way to make women’s integration into senior higher education positions easier. In Spain, Organic Act 3/20071 of 22 March on effective equality between women and men launched progressive norms governing gender issues, and the Spanish Science and Technology Act (2011) incorporated measures to promote effective equality in academic institutions. This paper evaluates how Spanish evaluation agencies’ compliance with implementing gender balance has affected the composition of evaluation committees and its impact on the advancement of women in science. Findings reveal some positive figures on women’s representation in recent decades, even though gender-balanced committees do not show any clear evidence of causing this effect. There seems to be no correlation between gender-balanced committees and women’s success rates, suggesting intermediate variables affect women’s low participation in competitive submissions. It explores several factors concerning two agencies’ evaluation procedures, such as formality and transparency, direct/multiple gatekeeping processes, the influence of epistemic cultures, cohorts and confidence of female candidates.Postprint (author's final draft

How to diagnose equal opportunities between women and men in organizations

Gender equality is now a matter that concerns all European countries. Despite the great effort made by governments and the progress of laws, gender discrimination still exists in family, social, cultural, political and economic spheres. Even today, it is rare to find women at the top level in companies. The path to equal opportunities is long and the only way to improve the situation is by means of appropriate equal opportunities plans. An essential part of the process of designing and implementing such action plans involves diagnosing the situation in a company. In this paper, an innovative indicator model is proposed. A review of numerous international private and public equal opportunities plans led to the design of a model to carry out a diagnose to identify all areas that could be corrected or improved by implementing specific measures, leading the company to deliver real equal opportunities policies. The indicator model is designed for the present historical context, though it is flexible enough to be adapted to each age and situation. The indicator model, which is original, will help companies carrying out one of the most important and essential parts of the process of designing and implementing and equal opportunities plan. Moreover, taking the indicator model companies ensure that all the relevant features are coveredPeer Reviewe

Compulsory equal opportunities plans: Advantages of equal opportunities between women and men for companies

La Ley de Igualdad Efectiva de mujeres y hombres, aprobada en España en 2007, establece la obligatoriedad de elaborar e implantar planes de igualdad de oportunidades a aquellas empresas con más de 250 trabajadores. La relación “coste-beneficio” de la igualdad de oportunidades (relación entre el nivel de igualdad de oportunidades en una empresa y sus resultados) es un tema que no ha sido aún explorado y, por ello, las empresas deben autoconvencerse de la conveniencia de implantar planes de igualdad por medio de argumentos no cuantitativos. En este artículo se discuten las principales ventajas que puede ofrecer a las empresas la igualdad de oportunidades entre mujeres y hombres y se ofrecen criterios y herramientas para su aplicación.The Equal Opportunities Spanish Law (from 2007), establishes that those companies with more than 250 workers have to design and implement an equal opportunities plan between women and men. Since the “cost-benefit” relation of equal opportunities has not been yet studied, companies have to convince themselves about the convenience of designing and adopting an equal opportunities plan by means of non quantitative reasons. In this paper the main advantages of equal opportunities for companies are discussed, and some criteria are offered for its application.Peer Reviewe

Situació i anàlisi de la igualtat d'oportunitats de gènere (IOG) al DOE

Preprin

Autonomous metabolic reprogramming and oxidative stress characterize endothelial dysfunction in acute myocardial infarction

Background: Compelling evidence has accumulated on the role of oxidative stress on the endothelial cell (EC) dysfunction underlying acute coronary syndrome. However, unveiling the underlying metabolic determinants has been hampered by the scarcity of appropriate cell models to address cell-autonomous mechanisms of ED dysfunction. Methods: We have generated endothelial cells derived from thrombectomy specimens from patients affected with acute myocardial infarction (AMI) and conducted phenotypical and metabolic characterization, focused on central carbon metabolism. Results: AMI-derived endothelial cells (AMIECs), but not control healthy coronary endothelial cells, display impaired growth, migration and tubulogenesis. Metabolically, AMIECs displayed augmented reactive oxygen species (ROS) and glutathione intracellular content, along with a diminished glucose consumption coupled to high lactate production. Consistent with diminished glycolysis in AMIECs, the protein levels of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase type 3, PFKFB3, were downregulated. In contrast, PFKFB4 levels were upregulated, suggesting a shunting of glycolysis towards the pentose phosphate pathway (PPP), supported by upregulation in AMIECs of G6PD, the key enzyme in the oxidative branch of the PPP. Further, the glutaminolytic enzyme GLS was upregulated in AMIECs, providing a mechanistic explanation for the observed increase in glutathione content. Finally, AMIECs displayed a significantly higher mitochondrial membrane potential than control ECs, which, together with high ROS levels, suggest a highly coupled mitochondrial activity in patient ECs. Conclusions: We suggest high mitochondrial proton coupling underlies the abnormally high production of ROS, balanced by PPP- and glutaminolysis-driven synthesis of glutathione, as a primary, cell-autonomous abnormality driving EC dysfunction in AMI. Funding: European Commission Horizon 2020; CIBER- Carlos III National Institute of Health, Spain; Ministerio de Economia y Competitividad (MINECO) and Ministerio de Ciencia e Innovación, Spain; Generalitat de Catalunya-AGAUR, Catalonia; Plataforma Temática Interdisciplinar Salud Global (PTI-SG), Spain; British Heart Foundation, UK. </p

Versican accumulation drives Nos2 induction and aortic disease in Marfan syndrome via Akt activation

Aortic aneurysm; Marfan syndrome; VersicanAneurisma aòrtic; Síndrome de Marfan; VersicanAneurisma aortico; Síndrome de Marfan; VersicanThoracic aortic aneurysm and dissection (TAAD) is a life-threatening condition associated with Marfan syndrome (MFS), a disease caused by fibrillin-1 gene mutations. While various conditions causing TAAD exhibit aortic accumulation of the proteoglycans versican (Vcan) and aggrecan (Acan), it is unclear whether these ECM proteins are involved in aortic disease. Here, we find that Vcan, but not Acan, accumulated in Fbn1C1041G/+ aortas, a mouse model of MFS. Vcan haploinsufficiency protected MFS mice against aortic dilation, and its silencing reverted aortic disease by reducing Nos2 protein expression. Our results suggest that Acan is not an essential contributor to MFS aortopathy. We further demonstrate that Vcan triggers Akt activation and that pharmacological Akt pathway inhibition rapidly regresses aortic dilation and Nos2 expression in MFS mice. Analysis of aortic tissue from MFS human patients revealed accumulation of VCAN and elevated pAKT-S473 staining. Together, these findings reveal that Vcan plays a causative role in MFS aortic disease in vivo by inducing Nos2 via Akt activation and identify Akt signaling pathway components as candidate therapeutic targets.The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia e Innovación (MCIN) and the Pro CNIC Foundation), the CBMSO is supported by Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid. CBMSO and CNIC are Severo Ochoa Centers of Excellence (grants CEX2021-001154-S and CEX2020-001041-S, respectively) funded by MICIN/AEI/10.13039/501100011033. The project leading to these results has received funding from “La Caixa” Banking Foundation under project codes HR18-00068 (to MRC and JMR); Spanish Ministerio de Ciencia e Innovación grant RTI2018-099246-B-I00 (MICIU/AEI/FEDER, UE) to JMR, and grants PID2020-115217RB-100 and PID2021-122388OB-100 to MRC and JMR, respectively, funded by MCIN/AEI/10.13039/501100011033; Instituto de Salud Carlos III (CIBER-CV CB16/11/00264 and CB16/11/00479; and grants PI17/00381 to GT-T and PI21/00084 (co-funded by Fondo Europeo de Desarrollo Regional (FEDER)) to JFN); Fundacio La Marato TV3 (20151330 to JMR); Instituto de Investigación Sanitaria Marqués de Valdecilla (IDIVAL) (INNVAL 21/24) to JFN; The Marfan Foundation USA Faculty grant 2017 MRF/1701 (to JMR); Fundación MERCK-Fundación Española de Enfermedades Raras 2022 and V-Ayudas “Muévete por los que no pueden 2021” (to JO); and Spanish Ministerio de Ciencia e Innovación contracts FPI (BES-2016-077649) to MJR-R; Sara Borrell (CD18/00028) and Juan de la Cierva (IJC2020-044581-I) to MT; Ramón y Cajal (RYC2021-033343-I) to JO; and FPU (20/04814) to IA-R

Aortic disease in Marfan syndrome is caused by overactivation of sGC-PRKG signaling by NO

Aneurysm; Aortic diseases; Marfan syndromeAneurisma; Malalties aòrtiques; Síndrome de MarfanAneurisma; Enfermedades aórticas; Síndrome de MarfanThoracic aortic aneurysm, as occurs in Marfan syndrome, is generally asymptomatic until dissection or rupture, requiring surgical intervention as the only available treatment. Here, we show that nitric oxide (NO) signaling dysregulates actin cytoskeleton dynamics in Marfan Syndrome smooth muscle cells and that NO-donors induce Marfan-like aortopathy in wild-type mice, indicating that a marked increase in NO suffices to induce aortopathy. Levels of nitrated proteins are higher in plasma from Marfan patients and mice and in aortic tissue from Marfan mice than in control samples, indicating elevated circulating and tissue NO. Soluble guanylate cyclase and cGMP-dependent protein kinase are both activated in Marfan patients and mice and in wild-type mice treated with NO-donors, as shown by increased plasma cGMP and pVASP-S239 staining in aortic tissue. Marfan aortopathy in mice is reverted by pharmacological inhibition of soluble guanylate cyclase and cGMP-dependent protein kinase and lentiviral-mediated Prkg1 silencing. These findings identify potential biomarkers for monitoring Marfan Syndrome in patients and urge evaluation of cGMP-dependent protein kinase and soluble guanylate cyclase as therapeutic targets

Inserción laboral de las titulaciones de la subárea de tecnologías avanzadas de la producción

Esta comunicación presenta los principales resultados de una encuesta sobre inserción laboral de los titulados y tituladas universitarios de la subárea de tecnologías avanzadas de la producción, describiendo la situación laboral de estos titulados en el momento de contestar la encuesta, la rapidez de acceso al mercado de trabajo y sus condiciones laborales: ámbito de trabajo, sector de actividad, dimensión de la empresa, funciones desarrolladas mayoritariamente por estos titulados, tipo de contrato y retribución. También se describe el grado de satisfacción con los estudios realizados y con el trabajo actual. Se comparan los resultados obtenidos de la subárea de tecnologías avanzadas de la producción con los resultados de la totalidad de las personas tituladas del área técnica y del total de titulaciones. En todo el análisis se ha tenido en cuenta la perspectiva de género y se ponen de manifiesto diferencias en la rapidez de inserción entre mujeres y hombres y en la calidad de esta inserción.Postprint (author’s final draft

Circulating progenitor cells and vascular dysfunction in chronic obstructive pulmonary disease.

BACKGROUND: In chronic obstructive pulmonary disease (COPD), decreased progenitor cells and impairment of systemic vascular function have been suggested to confer higher cardiovascular risk. The origin of these changes and their relationship with alterations in the pulmonary circulation are unknown. OBJECTIVES: To investigate whether changes in the number of circulating hematopoietic progenitor cells are associated with pulmonary hypertension or changes in endothelial function. METHODS: 62 COPD patients and 35 controls (18 non-smokers and 17 smokers) without cardiovascular risk factors other than cigarette smoking were studied. The number of circulating progenitors was measured as CD45(+)CD34(+)CD133(+) labeled cells by flow cytometry. Endothelial function was assessed by flow-mediated dilation. Markers of inflammation and angiogenesis were also measured in all subjects. RESULTS: Compared with controls, the number of circulating progenitor cells was reduced in COPD patients. Progenitor cells did not differ between control smokers and non-smokers. COPD patients with pulmonary hypertension showed greater number of progenitor cells than those without pulmonary hypertension. Systemic endothelial function was worse in both control smokers and COPD patients. Interleukin-6, fibrinogen, high sensitivity C-reactive protein, vascular endothelial growth factor and tumor necrosis factor were increased in COPD. In COPD patients, the number of circulating progenitor cells was inversely related to the flow-mediated dilation of systemic arteries. CONCLUSIONS: Pulmonary and systemic vascular impairment in COPD is associated with cigarette smoking but not with the reduced number of circulating hematopoietic progenitors. The latter appears to be a consequence of the disease itself not related to smoking habit