Prevalencia de factores de riesgo cardiovascular clásicos en población adulta de Talca, Chile, 2005

Departamento de Bioquímica Clínica e Inmunohematología, Facultad de Ciencias de la Salud, Universidad de Talca, Talca, Chile. Instituto de Matemática y Física, Universidad de Talca, Talca, Chile. Departamento de Salud Pública, Facultad de Ciencias de la Salud, Universidad de Talca, Talca, Chile. Escuela de Psicología, Universidad de Talca, Talca, Chile.Background: Cardiovascular disease (CVD) has several traditional risk factors (RF), and some of them are potentially modifiable. Aim: To determine the prevalence of most common risk factors in adult population in Talca in Central Chile. Subjects and methods: We studied 1007 subjects aged 18 to 74 years (66% women), living in Talca, selected by a probability sampling. They answered a questionnaire and anthropometry, blood pressure, lipid profile and blood glucose were measured. Results: Thirty seven percent of subjects smoked, 70.1% had a body mass index over 25 kg/m2 and 41% had an abnormally high circumference. High blood pressure was found in 37% (36% of these subjects were unaware of this condition), 44.5% had hypercholesterolemia, 21.5% had low HDL cholesterol, 40.1% had hypertriglyceridemia and 26.3% had high blood glucose levels. Conclusions: There is a high prevalence of risk factors for CVD in adult population from Talca. The prevalence of risk factors is higher than that reported by the 2003 National Health Survery

Patrón de comportamiento tipo A, ira y enfermedades cardiovasculares (ECV) en población urbana chilena

Diaz, EM (Moyano Diaz, Emilio)1; Icaza, G (Icaza, Gloria); Mujica, V (Mujica, Veronica); Nunez, L (Nunez, Loreto); Leiva, E (Leiva, Elba); Vasquez, M (Vasquez, Marcela); Palomo, I (Palomo, Ivan)A worldwide raise in the number of cardiovascular disease (CVD) and the existence of a higher percentage in Maule (Chile) than the national media, and increased attention in the analysis of psychological factors motivate to analyze the Type A Behavior Pattern (TABP) and anger in relation to CVD. The sample was 1007 adults between 18 and 74 years old (citizens of Talca, Chile), mostly women. They provided information about their demographic details, eating habits and lifestyle, answered the Novaco's Anger inventory and the Retiro Scale of Type A Behavior (RSTAB), and also were taken measurements like weight, body mass index and blood pressure and blood tests related to risk factors to traditional cardiovascular diseases. The results show Overall, that the participants appear highly sedentary (79.9%) with relatively high levels of tabaquism (53.6%), and hypercholesterolemia (44.5%), overweight (40.7%) and obesity (32.6%). A quarter of the sample also presents hyperglycemic indexes, hypertension and TABP unequally distributed by sex. The absence of PCTA (or PCTB presence) appeared mostly associated with traditional cardiovascular risk factors (CRF). Regarding anger, women present more high than men (2.1% against 0.3%; c(2)(3) = 27.99,p<.0001), decreasing for both sexes with age, while also befall stroke by sex

Using the second-order information for reconfigurability analysis and design in the fault tolerant framework

The control reconfigurability measure defines the capability of a control system to allow recovery of performance when faults occur; therefore, it has been intended to be a tool for designing and synthesizing approaches in the fault tolerant control context. Reconfigurability depends on the controllability gramian, also known as the second-order information (SOI) in a broad sense. This paper proposes the assignation, by feedback, of the deterministic SOI in order to set the control reconfigurability of a given linear system. The theory concerned with this assignation is reviewed, then constructive theorems are given for finding constant feedback gains that approximate a required control reconfigurability for ease implementation. Also an unification of the reconfigurability measures proposed in the fault tolerance literature is given. Once the SOI is assigned by feedback, it can be computed online by using an identification method, which uses process input/output data. Results from simulation of the three tanks hydraulic benchmark, show that this approach can provide information about the system performance for fault tolerant purposes, thus online control reconfigurability computation and fault accommodation are considered. The approach presented in the paper gives an alternative for supervision taking into account the reconfigurability assigned by design

Role of platelets as mediators that link inflammation and thrombosis in atherosclerosis

Platelets, crucial mediators of the acute complications of atherosclerosis that cause life-threatening ischemic events at late stages of the disease, are also key effectors of inflammation throughout plaque development through their interaction with endothelial and immune cells in the injured vessel wall. During the first steps of atherosclerosis, blood inflammatory leukocytes interact with the damaged endothelium in areas rich in platelet aggregates. In late stages of the disease, platelets secrete several inflammatory molecules, even without forming aggregates. These molecules exacerbate the inflammation and induce the transition from chronic to acute disease, featuring increased instability of the atherosclerotic lesion that results in plaque rupture and thrombosis. Moreover, platelets play an important role in vascular wall remodeling induced by chronic inflammation by controlling vascular cell differentiation and proliferation. In this review, we discuss the role of platelets as cell mediators that link inflammation and thrombosis in atherosclerotic disease and their potential in the development of new therapeutic tools to fight cardiovascular disease.Work in the author’s laboratories is supported by Centro de Estudios en Alimentos Procesados (CEAP), Conicyt-Regional, Gore Maule, R09I2001, Talca, Chile (Proyecto Basal); The Spanish Ministry of Science and Innovation (MICINN) and the European Regional Development Fund (grant SAF2010-16044); Instituto de Salud Carlos III (ISCIII) (Red de Enfermedades Cardiovasculares [RECAVA], grant RD06/0014/0021). O.M.P. holds a Juan de la Cierva contract (MICINN). The CNIC is supported by the MICINN and the Pro-CNIC Foundation.S

Bases psicobiológicas de la adicción a cocaína

El principal mecanismo de acción de la cocaína es la inhibición de la recaptación de dopamina y noradrenalina, produciendo un aumento de estos neurotransmisores en la sinapsis. El consumo agudo de cocaína produce una serie de cambios bastante conocidos en el sistema cerebral de recompensa. Sin embargo, el consumo crónico, produce, además, otra serie de cambios a nivel molecular que llevan al sujeto desde una situación de consumo puntual, a una situación de dependencia. Se han propuesto diferentes teorías explicativas de este fenómeno como la sensibilización del incentivo, o la homeostasis y alostasis neuroquímica, planteamientos basados en el condicionamiento clásico y operante. Por otra parte, se ha señalado la intervención de diferentes moléculas y vías de segundos mensajeros, que producen, en última instancia, una serie de cambios neuronales mantenidos a muy largo plazo, probablemente permanentes, que se podrían relacionar con la vulnerabilidad a las recaídas, propia de la adicción a cocaína, incluso años después de abandonar el consumo

Endothelial damage, inflammation and immunity in chronic kidney disease

Chronic kidney disease (CKD) patients have an accelerated atherosclerosis, increased risk of thrombotic-ischemic complications, and excessive mortality rates when compared with the general population. There is also evidence of an endothelial damage in which the proinflammatory state, the enhanced oxidative stress, or the accumulation of toxins due to their reduced renal clearance in uremia play a role. Further, there is evidence that uremic endothelial cells are both involved in and victims of the activation of the innate immunity. Uremic endothelial cells produce danger associated molecular patterns (DAMPS), which by binding to specific pattern recognition receptors expressed in multiple cells, including endothelial cells, induce the expression of adhesion molecules, the production of proinflammatory cytokines and an enhanced production of reactive oxygen species in endothelial cells, which constitute a link between immunity and inflammation. The connection between endothelial damage, inflammation and defective immunity in uremia will be reviewed here

BVDV permissiveness and lack of expression of co-stimulatory molecules on PBMCs from calves pre-infected with BVDV

Bovine viral diarrhea virus (BVDV) has been detected in peripheral blood mononuclear cells (PBMCs) of immunocompetent animals, not being clear whether the development of a specific humoral immune response can prevent BVDV infection. The aim of this study was to evaluate the ability of non-cytopathic BVDV to replicate and produce infectious virus in PBMCs from calves pre-infected with BVDV and to elucidate the immunomodulatory effect of BVDV on these cells in an in vitro model. Quantification of virus was by quantitative PCR, while its replicative capacity and shedding into the extracellular environment was evaluated by viral titration. Apoptosis was assessed by flow cytometry analysis of annexin V and propidium iodide, and by expression of caspase-3/7. Flow cytometry was used to analyze the expression of CD14/CD11b/CD80, CD4/CD8/CD25, MHC-I/MHC-II and B-B2 markers. Our results showed that PBMCs from cattle naturally infected with BVDV were more susceptible to in vitro BVDV infection and showed a more severe apoptosis response than those from na\uefve animals. Non-cytopathic BVDV in vitro infection also resulted in a lack of effect in the expression of antigen presentation surface markers. All these findings could be related to the immunosuppressive capacity of BVDV and the susceptibility of cattle to this infection

Post-2020 biodiversity targets need to embrace climate change

Recent assessment reports by the Intergovernmental Panel on Climate Change (IPCC) and the Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services (IPBES) have highlighted the risks to humanity arising from the unsustainable use of natural resources. Thus far, land, freshwater, and ocean exploitation have been the chief causes of biodiversity loss. Climate change is projected to be a rapidly increasing additional driver for biodiversity loss. Since climate change and biodiversity loss impact human societies everywhere, bold solutions are required that integrate environmental and societal objectives. As yet, most existing international biodiversity targets have overlooked climate change impacts. At the same time, climate change mitigation measures themselves may harm biodiversity directly. The Convention on Biological Diversity's post-2020 framework offers the important opportunity to address the interactions between climate change and biodiversity and revise biodiversity targets accordingly by better aligning these with the United Nations Framework Convention on Climate Change Paris Agreement and the Sustainable Development Goals. We identify the considerable number of existing and proposed post- 2020 biodiversity targets that risk being severely compromised due to climate change, even if other barriers to their achievement were removed. Our analysis suggests that the next set of biodiversity targets explicitly addresses climate change-related risks since many aspirational goals will not be feasible under even lower-end projections of future warming. Adopting more flexible and dynamic approaches to conservation, rather than static goals, would allow us to respond flexibly to changes in habitats, genetic resources, species composition, and ecosystem functioning and leverage biodiversity's capacity to contribute to climate change mitigation and adaptation

The U-shaped relationship between parental age and the risk of bipolar disorder in the offspring: A systematic review and meta-analysis

Parenthood age may affect the risk for the development of different psychiatric disorders in the offspring, including bipolar disorder (BD). The present systematic review and meta-analysis aimed to appraise the relationship between paternal age and risk for BD and to explore the eventual relationship between paternal age and age at onset of BD. We searched the MEDLINE, Scopus, Embase, PsycINFO online databases for original studies from inception, up to December 2021. Random-effects meta-analyses were conducted. Sixteen studies participated in the qualitative synthesis, of which k = 14 fetched quantitative data encompassing a total of 13,424,760 participants and 217,089 individuals with BD. Both fathers [adjusted for the age of other parent and socioeconomic status odd ratio – OR = 1.29(95%C.I. = 1.13–1.48)] and mothers aged ≤ 20 years [(OR = 1.23(95%C.I. = 1.14–1.33)] had consistently increased odds of BD diagnosis in their offspring compared to parents aged 25–29 years. Fathers aged ≥ 45 years [adjusted OR = 1.29 (95%C.I. = 1.15–1.46)] and mothers aged 35–39 years [OR = 1.10(95%C.I. = 1.01–1.19)] and 40 years or older [OR = 1.2(95% C.I. = 1.02–1.40)] likewise had inflated odds of BD diagnosis in their offspring compared to parents aged 25–29 years. Early and delayed parenthood are associated with an increased risk of BD in the offspring. Mechanisms underlying this association are largely unknown and may involve a complex interplay between psychosocial, genetic and biological factors, and with different impacts according to sex and age range. Evidence on the association between parental age and illness onset is still tentative but it points towards a possible specific effect of advanced paternal age on early BD-onset

Early vascular endothelial complications after hematopoietic cell transplantation: Role of the endotheliopathy in biomarkers and target therapies development

This work aims to review the role of endothelial dysfunction underlying the main complications appearing early after autologous and allogeneic hematopoietic cell transplantation (HCT). The endothelial damage as the pathophysiological substrate of sinusoidal obstruction syndrome (SOS) is well established. However, there is growing evidence of the involvement of endothelial dysfunction in other complications, such as acute graft-versus-host disease (aGVHD) and transplant-associated thrombotic microangiopathy (TA-TMAs). Moreover, HCT-related endotheliopathy is not only limited to the HCT setting, as there is increasing evidence of its implication in complications derived from other cellular therapies. We also review the incidence and the risk factors of the main HCT complications and the biological evidence of the endothelial involvement and other linked pathways in their development. In addition, we cover the state of the art regarding the potential use of the biomarkers of endotheliopathy in the prediction, the early diagnosis, and the follow-up of the HCT complications and summarize current knowledge points to the endothelium and the other linked pathways described as potential targets for the prevention and treatment of HCT-complications. Lastly, the endothelium-focused therapeutic strategies that are emerging and might have a potential impact on the survival and quality of life of post-HCT-patients are additionally reviewed.Copyright © 2022 Moreno-Castaño, Salas, Palomo, Martinez-Sanchez, Rovira, Fernández-Avilés, Martínez, Cid, Castro, Escolar, Carreras and Diaz-Ricart