Effects of a 48-Day Home Quarantine during the Covid-19 Pandemic on the First Outdoor Running Session among Recreational Runners in Spain.

COVID-19-induced quarantine may lead to deleterious effects on health status as well as to impaired performance and increased injury risk when re-starting training after lockdown. We investigated the physical activity (PA) habits of recreational runners in Spain during a 48-day home quarantine during the COVID-19 pandemic and the characteristics of the first outdoor running session after confinement. A cross-sectional study, including a self-reported running questionnaire completed after the first outdoor running session after quarantine, was performed. Three hundred recreational runners (74% males; 60% 18-40 years old; most typical running experience >3 years, 10-30 km weekly running distance distributed in 3-4 sessions) were considered for analysis. Advanced runners ran, at least, 4 days/week and participated in running events. They performed significantly longer and more non-supervised weekly training sessions during confinement (p < 0.01 for both) than novice and amateur runners. Most runners performed their first outdoor running session on asphalt (65.3%) and ran 5 to 10 km (61%) at a pace above 5 min/km (60%), reporting no pain before (77%), during (64%), and 24 h after (76%) the session. Advanced runners performed a significantly longer running session, at a higher pace, and covered a greater distance (p < 0.01 for all) than novice and amateur runners, while enjoyment and motivation tended to be significantly higher when runners' level increased (p < 0.05). Higher training levels prior to and during confinement may lower the collateral effects (e.g., detraining, injury risk) of home quarantine when runners return to previous PA levels.

Treatment directed to signalling molecules in patients with advanced differentiated thyroid cancer.

Mutation detection in samples from thyroid cancer with the addition of BRAF mutation, and also the detection of RAS, RET/PTC, and PAX8/PPARγ mutations, may also contribute to cancer diagnosis. On the other hand, the MAPK/ERK (mitogen-activated protein kinase/extracellular signal-regulated kinase signaling pathway) and PI3K/Akt (lipid kinase phoshoinositid-3-kinase signaling pathway) play an important role in the transmission of cell signals. The genes, coding the signaling cascade proteins (RET, RAS, BRAF, PI3K, PTEN, AKT), are mutated or aberrantly expressed in thyroid cancer derived from follicular thyroid cells. Genetic and epigenetic alternations, concerning MAPK/ERK and PI3K/Akt signaling pathways, contribute to their activation and interaction as a consequence of malignant follicular cell transformation. The understanding of this molecular mechanism provides access to novel molecular prognostic and therapeutic strategies for inhibiting the oncogenic activity of the signaling pathways. This ability to investigate tumour biology allows for the selection of different drugs. Nowadays the most relevant are treatments directed to tyrosine kinase receptors that bind for a wide variety of ligands and are frequently mutated and induce a constitutive activation such that a chimerical protein expression takes place in follicular cells in the domain of RET, as well as in other receptors. Many molecules such as: motesanib, sorafenib, vandetanib, sunitinib, XL-184, imatinib, axitinib, pazopanib, lenvatinib, combretastatin, gefitinib, cetuximab, bortezomib and thiazoldonedione have been developed. Some of them also can act in receptors of vascular endothelial growth factor and epidermal growth factor receptors. Information obtained through cytological or biopsy samples permits the study of complex metabolic or genetic pathways, thus providing researchers with a high throughput tool for elucidating changes in the global expression patterns seen in tumour cells and allowing for different therapeutic strategies in thyroid cancer which take into account the predominant altered pathways observed in these samples.

[Pediatric cardiology and congenital heart disease: from fetus to adult]. / Cardiología pediátrica y cardiopatías congénitas: del feto al adulto.

This article contains a review of some of the most important publications on congenital heart disease and pediatric cardiology that appeared in 2010 and up until September 2011. Of particular interest were studies on demographic changes reported in this patient population and on the need to manage the patients' transition from the pediatric to the adult cardiology department. This transition has given rise to the appearance of new areas of interest: for example, pregnancy in women with congenital heart disease, and the effect of genetic factors on the etiology and transmission of particular anomalies. In addition, this review considers some publications on fetal cardiology from the perspective of early diagnosis and, if possible, treatment. There follows a discussion on new contributions to Eisenmenger's syndrome and arrhythmias, as well as on imaging techniques, interventional catheterization and heart transplantation. Finally, there is an overview of the new version of clinical practice guidelines on the management of adult patients with congenital heart disease and of recently published guidelines on pregnancy in women with heart disease, both produced by the European Society of Cardiology.

Cardiología pediátrica y cardiopatías congénitas: del feto al adulto / Pediatric cardiology and congenital heart disease: from fetus to adult

Presentamos una revisión de algunos de los artículos más significativos publicados en el área de las cardiopatías congénitas y la cardiología pediátrica durante 2010 y hasta septiembre de 2011, con especial interés en los relacionados con los cambios demográficos que se han producido en esta población y con la necesidad de realizar la transición de estos pacientes desde los servicios de cardiología pediátrica a los de adulto. Ello ha dado lugar a la aparición de nuevas áreas de interés, como el embarazo en mujeres con una cardiopatía congénita y el papel que los factores genéticos pueden tener en la etiología y la transmisión de determinadas anomalías. Asimismo, y con el objetivo de precocidad diagnóstica y, de ser posible, terapéutica, se revisan algunos artículos relacionados con la cardiología fetal. Seguidamente se mencionan las nuevas aportaciones en el síndrome de Eisenmenger y las arritmias, así como en técnicas de imagen, cateterismo intervencionista y trasplante cardiaco; finalmente se alude a la nueva versión de las guías de práctica clínica sobre el manejo del paciente adulto con una cardiopatía congénita y a la recientemente publicada guía sobre el embarazo de mujeres con cardiopatía, ambas procedentes de la Sociedad Europea de Cardiología (AU)

This article contains a review of some of the most important publications on congenital heart disease and pediatric cardiology that appeared in 2010 and up until September 2011. Of particular interest were studies on demographic changes reported in this patient population and on the need to manage the patients ‘transition from the pediatric to the adult cardiology department. This transition has given rise to the appearance of new areas of interest: for example, pregnancy in women with congenital heart disease, andthe effect of genetic factors on the etiology and transmission of particular anomalies. In addition, this review considers some publications on fetal cardiology from the perspective of early diagnosis and, if possible, treatment. There follows a discussion on new contributions to Eisenmenger’s syndrome and arrhythmias, as well as on imaging techniques, interventional catheterization and heart transplantation. Finally, there is an overview of the new version of clinical practice guidelines on the management of adult patients with congenital heart disease and of recently published guidelines on pregnancy in women with heart disease, both produced by the European Society of Cardiology (AU)

Diagnostic and prognostic markers in differentiated thyroid cancer.

The MAPK/ERK (mitogen-activated protein kinase/extracellular signal- regulated kinase signaling pathway) and PI3K/Akt (lipid kinase phoshoinositide-3-kinase signaling pathway) play an important role in transmission of cell signals through transduction systems as ligands, transmembrane receptors and cytoplasmic secondary messengers to cell nucleus, where they influence the expression of genes that regulate important cellular processes: cell growth, proliferation and apoptosis. The genes, coding the signaling cascade proteins (RET, RAS, BRAF, PI3K, PTEN, AKT), are mutated or aberrantly expressed in thyroid cancer derived from follicular thyroid cell. Genetic and epigenetic alternations, concerning MAPK/ERK and PI3K/Akt signaling pathways, contribute to their activation and interaction in consequence of malignant follicular cell transformation. Moreover, it is additionally pointed out that genetic, as well as epigenetic DNA changing via aberrant methylation of several tumor suppressor and thyroid-specific genes is associated with tumor aggressiveness, being a jointly responsible mechanism for thyroid tumorigenesis. In the present manuscript the currently developed diagnostic and prognostic genetic/epigenetic markers are presented; the understanding of this molecular mechanism provides access to novel molecular therapeutic strategies.

The outer membrane protein X from Escherichia coli exhibits immune properties.

Outer membrane proteins (OMP) are expressed in Gram-negative bacterial cell wall. OmpA from Klebsiella pneumoniae (KpOmpA) has been shown to bind and to activate selectively antigen presenting cells (APCs), eliciting protective CTL responses. In this study, we investigated whether OmpX, another member of the OMP family and structurally related to OmpA, exhibits the same immune properties. Using recombinant OmpX from Escherichia coli (EcOmpX), we report that EcOmpX binds to and is internalized by human APCs. However, EcOmpX does not activate APCs. EcOmpX acts as an efficient carrier protein as it induces a potent and Th1/Th2 mixed anti-TNP humoral response. However, adjuvant is required to generate a protective anti-tumoral immune response in mice injected with a tumor model antigen coupled to EcOmpX. Collectively, these data show that EcOmpX is recognized by innate cells but does not activate them, suggesting that EcOmpX does not provide a signal danger to APCs. In conclusion, this study provides information on the molecular mechanisms involved in the recognition and activation of innate cells by bacterial outer membrane proteins.

Development and function of the human fetal adrenal cortex.

The development and function of the primate adrenal cortex are characterized by rapid growth, high steroidogenic activity, and a particular morphological appearance. The fetal adrenal glands grow rapidly and exponentially and at term are similar in weight to adult adrenals. From birth to 1 year their mass is reduced as they undergo a process of differentiation. Growth then remains slow until age 7 years. Thereafter, growth accelerates and the adrenals reach adult weight by the end of puberty. In the first trimester of gestation, fetal adrenal growth is thought to be independent of adrenocorticotropic hormone (ACTH), but after 15 weeks, ACTH is absolutely required for normal morphological and functional development. Other factors of fetal and/or placental origin, acting independently of or in conjunction with ACTH, are also required. Basic fibroblast growth factor, epidermal growth factor/transforming growth factor beta, and insulin-like growth factor (IGF)-I and -II, all acting in an autocrine and/or paracrine fashion, have been postulated to stimulate fetal adrenal cell proliferation. Corticotropin-releasing hormone may also play an important role in primate fetal adrenal function, primarily at the end of gestation. Finally, the estrogens are also important in the development of the pituitary-adrenal axis in primates.