Biografia de D. Martin Fernandez de Navarrete

Tít. tomado de p. [3] y mención de responsabilidad de la últimaEn la última p. figura 184

Synthetic Slag Production Method Based on a Solid Waste Mix Vitrification for the Manufacturing of Slag-Cement

Herein an innovative process to develop a potential vitreous material with cementing properties is proposed. This process paves a production path through melting industrial waste and subsequently cooling the casting in water. The idea erases the need to reduce the environmental impact of the cement industry in terms of natural resources consumption as well as the re-utilization of abandoned wastes from other industries. The recycled industrial wastes were selected according to the amount of waste produced in the industrial field and its suitable chemical composition, such as construction and demolition waste and/or shells from shellfish. As a main result, the mechanical properties showed by our novel material were worse than those reported by blast furnace slag (25–28 MPa for two different proportions) for seven days and better (43–52 MPa for two different proportions) for 28 days. The rest of the properties evaluated were in agreement with the standards’ requirements. Hence, this novel process would help to minimize the environmental impact of these wastes at the same time that their use in the cement industry would reduce the consumption of raw materials.Gobierno de España ITC-2011101

Ephemerides barometrico-medicas matritenses, para el mas puntual, y exacto calculo de las observaciones que han de ilustrar la Historia Natural, y Medica de España

Tablas metereológica

MiRNA expression profile of human subcutaneous adipose and during adipocyte differentiation

This is an open-access article distributed under the terms of the Creative Commons Attribution License.-- et al.[Background]: Potential regulators of adipogenesis include microRNAs (miRNAs), small non-coding RNAs that have been recently shown related to adiposity and differentially expressed in fat depots. However, to date no study is available, to our knowledge, regarding miRNAs expression profile during human adipogenesis. Thereby, the aim of this study was to investigate whether miRNA pattern in human fat cells and subcutaneous adipose tissue is associated to obesity and co-morbidities and whether miRNA expression profile in adipocytes is linked to adipogenesis. [Methodology/Principal Findings]: We performed a global miRNA expression microarray of 723 human and 76 viral mature miRNAs in human adipocytes during differentiation and in subcutaneous fat samples from non-obese (n=6) and obese with (n=9) and without (n=13) Type-2 Diabetes Mellitus (DM-2) women. Changes in adipogenesis-related miRNAs were then validated by RT-PCR. Fifty of 799 miRNAs (6.2%) significantly differed between fat cells from lean and obese subjects. Seventy miRNAs (8.8%) were highly and significantly up or down-regulated in mature adipocytes as compared to pre-adipocytes. Otherwise, 17 of these 799 miRNAs (2.1%) were correlated with anthropometrical (BMI) and/or metabolic (fasting glucose and/or triglycerides) parameters. We identified 11 miRNAs (1.4%) significantly deregulated in subcutaneous fat from obese subjects with and without DM-2. Interestingly, most of these changes were associated with miRNAs also significantly deregulated during adipocyte differentiation. [Conclusions/Significance]: The remarkable inverse miRNA profile revealed for human pre-adipocytes and mature adipocytes hints at a closely crosstalk between miRNAs and adipogenesis. Such candidates may represent biomarkers and therapeutic targets for obesity and obesity-related complications.This work was supported by research grants from the Ministerio de Educación y Ciencia (MEC) (SAF2008-02073), the Instituto de Salud Carlos III (CIBERObN, CB06/03/0010), and the Hospital Dr. Josep Trueta de Girona.Peer reviewe

Decreased STAMP2 expression in association with visceral adipose tissue dysfunction

10 páginas, 6 figuras, 2 tablas.-- et al.[Context]: Six-transmembrane protein of prostate 2 (STAMP2) is a counter-regulator of inflammation and insulin resistance according to findings in mice. However, there have been contradictory reports in humans. [Objective]: We aimed to explore STAMP2 in association with inflammatory and metabolic status of human obesity. [Design, Patients, and Methods]: STAMP2 gene expression was analyzed in adipose tissue samples (171 visceral and 67 sc depots) and during human preadipocyte differentiation. Human adipocytes were treated with macrophage-conditioned medium, TNF-α, and rosiglitazone. [Results]: In visceral adipose tissue, STAMP2 gene expression was significantly decreased in obese subjects, mainly in obese subjects with type 2 diabetes. STAMP2 gene expression and protein were significantly and inversely associated with obesity phenotype measures (body mass index, waist, hip, and fat mass) and obesity-associated metabolic disturbances (systolic blood pressure and fasting glucose). In addition, STAMP2 gene expression was positively associated with lipogenic (FASN, ACC1, SREBP1, THRSP14, TRα, and TRα1), CAV1, IRS1, GLUT4, and CD206 gene expression. In sc adipose tissue, STAMP2 gene expression was not associated with metabolic parameters. In both fat depots, STAMP2 gene expression in stromovascular cells was significantly higher than in mature adipocytes. STAMP2 gene expression was significantly increased during the differentiation process in parallel to adipogenic genes, being increased in preadipocytes derived from lean subjects. Macrophage-conditioned medium (25%) and TNF-α (100 ng/ml) administration increased whereas rosiglitazone (2 μM) decreased significantly STAMP2 gene expression in human differentiated adipocytes. [Conclusions]: Decreased STAMP2 expression (mRNA and protein) might reflect visceral adipose dysfunction in subjects with obesity and type 2 diabetes.Peer reviewe

Circulating omentin concentration increases after weight loss

<p>Abstract</p> <p>Background</p> <p>Omentin-1 is a novel adipokine expressed in visceral adipose tissue and negatively associated with insulin resistance and obesity. We aimed to study the effects of weight loss-induced improved insulin sensitivity on circulating omentin concentrations.</p> <p>Methods</p> <p>Circulating omentin-1 (ELISA) concentration in association with metabolic variables was measured in 35 obese subjects (18 men, 17 women) before and after hypocaloric weight loss.</p> <p>Results</p> <p>Baseline circulating omentin-1 concentrations correlated negatively with BMI (r = -0.58, p < 0.001), body weight (r = -0.35, p = 0.045), fat mass (r = -0.67, p < 0.001), circulating leptin (r = -0.7, p < 0.001) and fasting insulin (r = -0.37, p = 0.03). Circulating omentin-1 concentration increased significantly after weight loss (from 44.9 ± 9.02 to 53.41 ± 8.8 ng/ml, p < 0.001). This increase in circulating omentin after weight loss was associated with improved insulin sensitivity (negatively associated with HOMA value and fasting insulin, r = -0.42, p = 0.02 and r = -0.45, p = 0.01, respectively) and decreased BMI (r = -0.54, p = 0.001).</p> <p>Conclusion</p> <p>As previously described with adiponectin, circulating omentin-1 concentrations increase after weight loss-induced improvement of insulin sensitivity.</p

The MRC1/CD68 ratio is positively associated with adipose tissue lipogenesis and with muscle mitochondrial gene expression in humans

This is an open-access article distributed under the terms of the Creative Commons Attribution License.[Background]: Alternative macrophages (M2) express the cluster differentiation (CD) 206 (MCR1) at high levels. Decreased M2 in adipose tissue is known to be associated with obesity and inflammation-related metabolic disturbances. Here we aimed to investigate MCR1 relative to CD68 (total macrophages) gene expression in association with adipogenic and mitochondrial genes, which were measured in human visceral [VWAT, n = 147] and subcutaneous adipose tissue [SWAT, n = 76] and in rectus abdominis muscle (n = 23). The effects of surgery-induced weight loss were also longitudinally evaluated (n = ).[Results]: MCR1 and CD68 gene expression levels were similar in VWAT and SWAT. A higher proportion of CD206 relative to total CD68 was present in subjects with less body fat and lower fasting glucose concentrations. The ratio MCR1/CD68was positively associated with IRS1gene expression and with the expression of lipogenic genes such as ACACA, FASN and THRSP, even after adjusting for BMI. The ratio MCR1/CD68 in SWAT increased significantly after the surgery-induced weight loss (+44.7%; p = 0.005) in parallel to the expression of adipogenic genes. In addition, SWAT MCR1/CD68ratio was significantly associated with muscle mitochondrial gene expression (PPARGC1A, TFAM and MT-CO3). AT CD206 was confirmed by immunohistochemistry to be specific of macrophages, especially abundant in crown-like structures. [Conclusion]: A decreased ratio MCR1/CD68 is linked to adipose tissue and muscle mitochondrial dysfunction at least at the level of expression of adipogenic and mitochondrial genes. © 2013 moreno-navarrete et al.This work was supported by grant SAF-2009-10461 and grant PI11-00214 from the Ministerio de Economía y Competitividad, Spain.Peer Reviewe

Antenatal Fear of Childbirth as a Risk Factor for a Bad Childbirth Experience

Giving birth is one of the most impressive experiences in life. However, many pregnant women suffer from fear of childbirth (FOC) and experience labour in very different ways, depending on their personality, previous life experiences, pregnancy, and birth circumstances. The aim of this study was to analyse how fear of childbirth affects the childbirth experience and to assess the related consequences. For this, a descriptive cross-sectional study was carried out in a sample of 414 women between 1 July 2021 and 30 June 2022. The Birth Anticipation Scale (BAS) was used to measure fear of childbirth and the Childbirth Experience Questionnaire (CEQ-E) was applied to measure satisfaction with the childbirth experience. Fear of childbirth negatively and significantly predicted the childbirth experience. In addition, women who were more fearful of childbirth were found to have worse obstetric outcomes and a higher likelihood of having a caesarean delivery (p = 0.008 C. I 95%). Fear behaved as a risk factor for the birth experience, so the greater the fear, the higher the risk of having a worse birth experience (OR 1.1). Encouraging active listening and support strategies may increase pregnant women's confidence, thus decreasing their fear of the process and improving their childbirth experience

Embryology of the abnormally high origin of a coronary artery (High Take-Off) in a mouse model.

High take-off (HTO) is a rare congenital coronary artery anomaly associated with sudden cardiac death. The coronary ostium is located in the ascending aorta above the sinotubular junction. The morphogenetic defect leading to HTO is currently unknown. Our group has shown occurrence of HTO in different strains of laboratory mice, including C57Bl/6 strain with 58% incidence of HTO and Balb/c strain with null incidence. Our aim is to investigate the aetiology of HTO, using C57BL/6 and Balb/c mice strains as experimental models. The process of coronariogenesis was examined in E13.5 and E14.5 mouse embryos of C57Bl/6 (n=27) and Balb/c (n=23) strains. We used histochemistry and immunohistochemistry with specific markers for the vascular plexuses involved in the formation of coronary arteries (PROX1 and ERG 1/2/3). In the mouse embryo, coronary ostia develop at approximately stage E14.5. The location of the ostia is determined by the confluence of two vascular plexuses. The transient lymphatic subepicardial aortic plexus migrates from the pharyngeal region, invading the subepicardial space of the intrapericardial thoracic arteries at around E13.5. The primary or ventricular plexus, which constitutes the future coronary vascular network, forms in situ, reaching the embryonic cardiac outflow tract at around E14. Eighteen of the 27 (66.7%) C57Bl/6 embryos showed an exacerbated subepicardial aortic plexus compared to the 23 Balb/c embryos, in which the subepicardial aortic plexus exhibited a normal size. These results suggest that the embryonic origin of HTO could be due to a defect in the growth of the subepicardial aortic plexus, resulting in an exacerbated vessel network. This overgrowth seems to alter the invasion and connection of the primary plexus to the aortic root for the establishment of the ostia and coronary trunks. From a biomedical viewpoint, it would be of great interest to investigate the molecular mechanisms underlying the overgrowth of the aortic plexus.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech; PI-0530-2019 (Consejería de Salud y Familias, Junta de Andalucía); UMA20-FEDERJA-041 (Junta de Andalucía y Fondos FEDER); PROYEXCEL_01009 (PAIDI, Junta de Andalucía); PRE2018-083176 (Ministerio de Ciencia, Innovación y Universidades), CONT-FIMABIS-0610/2023 (Junta de Andalucía)

Experimental evidence of the genetic hypothesis on the etiology of bicuspid aortic valve aortopathy in the hamster model.

Bicuspid aortopathy occurs in approximately 50% of patients with bicuspid aortic valve (BAV), the most prevalent congenital cardiac malformation. Although different molecular players and etiological factors (genetic and hemodynamic) have been suggested to be involved in aortopathy predisposition and progression, clear etiophysiopathological mechanisms of disease are still missing. The isogenic (genetically uniform) hamster (T) strain shows 40% incidence of BAV, but aortic dilatations have not been detected in this model. We have performed comparative anatomical, histological and molecular analyses of the ascending aorta of animals with tricuspid aortic valve (TAV) and BAV from the T strain (TTAV and TBAV, respectively) and with TAV from a control strain (HTAV). Aortic diameter, smooth muscle apoptosis, elastic waviness, and Tgf-β and Fbn-2 expression were significantly increased in T strain animals, regardless of the valve morphology. Strain and aortic valve morphology did not affect Mmp-9 expression, whereas Mmp-2 transcripts were reduced in BAV animals. eNOS protein amount decreased in both TBAV and TTAV compared to HTAV animals. Thus, histomorphological and molecular alterations of the ascending aorta appear in a genetically uniform spontaneous hamster model irrespective of the aortic valve morphology. This is a direct experimental evidence supporting the genetic association between BAV and aortic dilatation. This model may represent a population of patients with predisposition to BAV aortopathy, in which increased expression of Tgf-β and Fbn-2 alters elastic lamellae structure and induces cell apoptosis mediated by eNOS. Patients either with TAV or BAV with the same genetic defect may show the same risk to develop bicuspid aortopathy.This work was supported by Consejería de Salud y Familias, Junta de Andalucía (PI-0530-2019), Consejería de Economía y Conocimiento, Junta de Andalucía (UMA20-FEDERJA-041), Ministerio de Ciencia e Innovación (grants CGL2017-85090- P and PT20/00101, fellowship PRE2018-083176 to MS-N), and FEDER funds.S