Asthma, obesity and diet

El asma y la obesidad son dos trastornos de gran impacto en la salud pública que han aumentado su prevalencia en los últimos años. Numerosos estudios han relacionado ambas entidades. La mayoría de los estudios prospectivos demuestran que la obesidad es un factor de riesgo para el diagnóstico “de novo” de asma. Además, los resultados de diversos estudios sugieren que así como la ganancia de peso aumenta el riesgo de asma, la pérdida mejora su evolución. En general, los estudios prospectivos encuentran una asociación positiva entre el índice de masa corporal (IMC) basal y el posterior desarrollo de asma, lo que sugiere que es el exceso de peso el que podría favorecer el desarrollo de asma, aunque estos resultados no son tan concluyentes cuando se estudia la asociación entre hiperreactividad bronquial con el IMC. Existen distintos factores que podrían explicar esta asociación. La obesidad es capaz de reducir la compliance pulmonar, los volúmenes pulmonares y el diámetro de de las vías respiratorias periféricas, así como alterar los volúmenes sanguíneos pulmonares y la relación ventilación- perfusión. Además, el aumento del funcionamiento normal del tejido adiposo en sujetos obesos conduce a un estado proinflamatorio sistémico, que produce un aumento de las concentraciones séricas de numerosas citoquinas, fracciones solubles de sus receptores y quimiocinas. Muchos de estos mediadores son sintetizados y secretados por células del tejido adiposo y reciben el nombre genérico de adipocinas, entre las que se incluyen IL-6, IL-10, eotaxina, TNF- , TGF- 1, PCR, leptina y adiponectina. Por último, se han identificado regiones específicas del genoma humano que están relacionadas tanto con el asma como con la obesidad. La mayoría de los estudios apuntan a que la obesidad es capaz de aumentar la prevalencia y la incidencia de asma, aunque este efecto parece ser moderado. El tratamiento de los asmáticos obesos debe incluir un programa de control de peso.Asthma and obesity have a considerable impact on public health and their prevalence has increased in recent years. Numerous studies have linked both disorders. Most prospective studies show that obesity is a risk factor for asthma and have found a positive correlation between baseline body mass index (BMI) and the subsequent development of asthma, although these results are not conclusive when studying the association between airway hyperresponsiveness with BMI. Furthermore, several studies suggest that whereas weight gain increases the risk of asthma, weight loss improves the course of the illness. Different factors could explain this association. Obesity is capable of reducing pulmonary compliance, lung volumes and the diameter of peripheral respiratory airways as well as affecting the volume of blood in the lungs and the ventilation-perfusion relationship. Furthermore, the increase in the normal functioning of adipose tissue in obese subjects leads to a systemic proinflammatory state, which produces a rise in the serum concentrations of several cytokines, the soluble fractions of their receptors and chemokines. Many of these mediators are synthesized and secreted by cells from adipose tissue and receive the generic name of adipokines, including IL-6, IL-10, eotaxin, TNF- , TGF- 1, PCR, leptin y adiponectin. Finally, specific regions of the human genome which are related to both asthma and obesity have been identified. Most studies point out that obesity is capable of increasing the prevalence and incidence of asthma, although this effect appears to be modest. The treatment of obese asthmatics must include a weight control progra

Acute febrile illness is associated with Rickettsia spp infection in dogs

BACKGROUND: Rickettsia conorii is transmitted by Rhipicephalus sanguineus ticks and causes Mediterranean Spotted Fever (MSF) in humans. Although dogs are considered the natural host of the vector, the clinical and epidemiological significance of R. conorii infection in dogs remains unclear. The aim of this prospective study was to investigate whether Rickettsia infection causes febrile illness in dogs living in areas endemic for human MSF. METHODS: Dogs from southern Italy with acute fever (n = 99) were compared with case–control dogs with normal body temperatures (n = 72). Serology and real-time PCR were performed for Rickettsia spp., Ehrlichia canis, Anaplasma phagocytophilum/A. platys and Leishmania infantum. Conventional PCR was performed for Babesia spp. and Hepatozoon spp. Acute and convalescent antibodies to R. conorii, E. canis and A. phagocytophilum were determined. RESULTS: The seroprevalence rates at first visit for R. conorii, E. canis, A. phagocytophilum and L. infantum were 44.8%, 48.5%, 37.8% and 17.6%, respectively. The seroconversion rates for R. conorii, E. canis and A. phagocytophilum were 20.7%, 14.3% and 8.8%, respectively. The molecular positive rates at first visit for Rickettsia spp., E. canis, A. phagocytophilum, A. platys, L. infantum, Babesia spp. and Hepatozoon spp. were 1.8%, 4.1%, 0%, 2.3%, 11.1%, 2.3% and 0.6%, respectively. Positive PCR for E. canis (7%), Rickettsia spp. (3%), Babesia spp. (4.0%) and Hepatozoon spp. (1.0%) were found only in febrile dogs. The DNA sequences obtained from Rickettsia and Babesia PCRs positive samples were 100% identical to the R. conorii and Babesia vogeli sequences in GenBank®, respectively. Febrile illness was statistically associated with acute and convalescent positive R. conorii antibodies, seroconversion to R. conorii, E. canis positive PCR, and positivity to any tick pathogen PCRs. Fourteen febrile dogs (31.8%) were diagnosed with Rickettsia spp. infection based on seroconversion and/or PCR while only six afebrile dogs (12.5%) seroconverted (P = 0.0248). The most common clinical findings of dogs with Rickettsia infection diagnosed by seroconversion and/or PCR were fever, myalgia, lameness, elevation of C-reactive protein, thrombocytopenia and hypoalbuminemia. CONCLUSIONS: This study demonstrates acute febrile illness associated with Rickettsia infection in dogs living in endemic areas of human MSF based on seroconversion alone or in combination with PCR

Neuroinflammation in the normal-appearing white matter (NAWM) of the multiple sclerosis brain causes abnormalities at the nodes of Ranvier

Changes to the structure of nodes of Ranvier in the normal-appearing white matter (NAWM) of multiple sclerosis (MS) brains are associated with chronic inflammation. We show that the paranodal domains in MS NAWM are longer on average than control, with Kv1.2 channels dislocated into the paranode. These pathological features are reproduced in a model of chronic meningeal inflammation generated by the injection of lentiviral vectors for the lymphotoxin-α (LTα) and interferon-γ (IFNγ) genes. We show that tumour necrosis factor (TNF), IFNγ, and glutamate can provoke paranodal elongation in cerebellar slice cultures, which could be reversed by an N-methyl-D-aspartate (NMDA) receptor blocker. When these changes were inserted into a computational model to simulate axonal conduction, a rapid decrease in velocity was observed, reaching conduction failure in small diameter axons. We suggest that glial cells activated by pro-inflammatory cytokines can produce high levels of glutamate, which triggers paranodal pathology, contributing to axonal damage and conduction deficits

Tight blood pressure control decreases apoptosis during renal damage

Tight blood pressure control decreases apoptosis during renal damage.BackgroundAn excess rate of apoptosis could lead to the gradual loss of renal mass. In this study, we investigated the role of apoptosis in the renal damage secondary to hypertension.MethodsSpontaneously hypertensive rats with 5/6 renal mass reduction (subtotal nephrectomy) were distributed to receive no-treatment, 200mg/L quinapril, 360mg/L losartan, or triple therapy (200mg/L hydralazine, 4mg/L reserpine, and 100mg/L hydrochlorothiazide) for 5weeks. Sham-operated spontaneously hypertensive rats served as controls. Age-matched Wistar-Kyoto (WKY) rats, with or without subtotal nephrectomy, were also studied.ResultsNontreated spontaneously hypertensive rats + subtotal nephrectomy developed proteinuria, glomerular sclerosis, and tubulointerstitial lesions. In comparison to spontaneously hypertensive rats, an increment in the number of [proliferating cell nuclear antigen (PCNA)]-positive and apoptotic [terminal deoxynucleotidyl transferase (Tdt)-mediated deoxyuridine triphosphate biotin nick end labeling (TUNEL)]-positive tubular and glomerular cells was observed. By contrast, WKY + subtotal nephrectomy rats showed less severe morphologic lesions, and only the number of proliferating cells increased. By Western blot, an up-regulation of renal Bax (apoptosis inducer) was noted both in spontaneously hypertensive rats + subtotal nephrectomy and WKY + subtotal nephrectomy rats. By contrast, Bcl-xL (apoptosis protector) was up-regulated in WKY + subtotal nephrectomy rats but not in spontaneously hypertensive rats + subtotal nephrectomy. The administration of appropriate doses of quinapril, losartan, or triple therapy to spontaneously hypertensive rats + subtotal nephrectomy normalized systolic blood pressure, partially prevented proteinuria, renal lesions and apoptosis, and decreased Bax, but no changes were noted in Bcl-xL. The Bax/Bcl-xL index was significantly increased in spontaneously hypertensive rats + subtotal nephrectomy compared to sham-operated spontaneously hypertensive rats and decreased in treated groups.ConclusionThe combination of renal mass reduction and hypertension caused severe renal lesions associated to an increment of apoptosis rate, mainly in tubular epithelial cells. Tight blood pressure control decreased the apoptosis rate and morphologic lesions. These studies suggest that changes in the expression of apoptosis-regulatory genes contribute to the progressive damage in hypertensive rats with renal mass reduction

Tracking the moisture transport from the Pacific towards Central and northern South America since the late 19th century

In this paper, we develop an instrumental index based on historical wind direction observations aimed to quantify the moisture transport from the tropical Pacific to Central and northern South America at a monthly scale. This transport is mainly driven by the so-called “Chocó jet”, a low-level westerly jet whose core is located at 5◦ N and 80◦ W. The Chocó jet is profoundly related to the dynamics of the Intertropical Convergence Zone in the eastern equatorial Pacific and it is responsible for up to 30 % of the total precipitation in these areas. We have been able to produce an index for this transport starting in the 19th century, adding almost a century of data to previous comparable indices. Our results indicate that the seasonal distribution of the precipitation in Central America has changed throughout the 20th century as a response to the changes in the Chocó jet, decreasing (increasing) its strength in July (September). Additionally, we have found that in general, the relationship between the Chocó jet and the El Niño–Southern Oscillation has been remarkably stable throughout the entire 20th century, a finding particularly significant because the stability of this relation is usually the basis of the hydrologic reconstructions in northern South America

Strontium hexaferrite platelets: a comprehensive soft X-ray absorption and Mössbauer spectroscopy study

IBERMÖSS-2019, Bilbao, 30-31 may 2019. --https://www.ehu.eus/es/web/ibermossmeetingStrontium ferrite (SFO, SrFe12O19) is a ferrite employed for permanent magnets due to its high magnetocrystalline anisotropy. Since its discovery in the mid-20th century, this hexagonal ferrite has become an increasingly important material both commercially and technologically, finding a variety of uses and applications. Its structure can be considered a sequence of alternating spinel (S) and rocksalt (R) blocks. All the iron cations are in the Fe3+ oxidation state and it has a ferrimagnetic configuration with five different cationic environments for the iron (three octahedral sites, a tetraedrical site and a bipiramidal site)[1,2]. We have studied the properties of SrFe 12O19 in the shape of platelets, up to several micrometers in width, and tens of nanometers thick, synthesized by a hydrothermal method. We have characterized the structural and magnetic properties of these platelets by Mössbauer spectroscopy, x-ray transmission microscopy (TMX), transmission electron microscopy (TEM), x-ray diffraction (XRD), vibrating-sample magnetometry (VSM), x-ray absorption spectroscopy (XAS), x-ray circular magnetic dichroism (XMCD) and photoemission electron microscopy (PEEM). To the best of our knowledge this is the first time that the x-ray absorption spectra at the Fe L 2,3 edges of this material in its pure form have been reported. The Mössbauer results recorded from these platelets both in the electron detection and transmission modes have helped to understand the iron magnetic moments determined by XMCD (Fig.1). The experimental results have been complemented with multiplet calculations aimed at reproducing the observed XAS and XMCD spectra at the Fe L 2,3 absorption edge, and by density functional theory (DFT) calculations to reproduce the oxygen K- absorption edge. Finally the domain pattern measured in remanence is in good agreement with micromagnetic simulations [3]

MEGARA-GTC stellar spectral library: I

MEGARA (Multi Espectrografo en GTC de Alta Resolucion para Astronomia) is an optical (3650-9750 Å), fibre-fed, medium-high spectral resolution (R = 6000, 12 000 and 20 000) instrument for the Gran Telescopio CANARIAS (GTC) 10.4-m telescope, commissioned in the summer of 2017, and currently in operation. The scientific exploitation of MEGARA requires a stellar spectra library to interpret galaxy data and to estimate the contribution of the stellar populations. In this paper, we introduce the MEGARA-GTC spectral library, detailing the rationale behind the building of this catalogue. We present the spectra of 97 stars (21 individual stars and 56 members of the globular cluster M15, which are both subsamples taken during the commissioning runs, and 20 stars from our ongoing GTC Open-Time programme). The spectra have R = 20 000 in the HR-R and HR-I set-ups, centred at 6563 and 8633 Å, respectively. We describe the procedures to reduce and analyse the data. Then, we determine the best-fitting theoretical models to each spectrum through a χ^(2) minimization technique, to derive the stellar physical parameters, and we discuss the results. We have also measured some absorption lines and indices. Finally, we introduce our project to complete the library and the data base in order to make the spectra available to the community

Mapping the ionized gas of the metal-poor HII galaxy PHL 293B with MEGARA

Here we report the first spatially resolved spectroscopic study for the galaxy PHL293B using the high-resolution GTC/MEGARA IFU. PHL293B is a local, extremely metal-poor, high ionization galaxy. This makes PHL 293B an excellent analogue for galaxies in the early Universe. The MEGARA aperture (~12.5''x 11.3'') covers the entire PHL 293B main body and its far-reaching ionized gas. We created and discussed maps of all relevant emission lines, line ratios and physical-chemical properties of the ionized ISM. The narrow emission gas appears to be ionized mainly by massive stars according to the observed diganostic line ratios, regardless of the position across the MEGARA aperture. We detected low intensity broad emission components and blueshifted absorptions in the Balmer lines (H$\alpha$,H$\beta$) which are located in the brightest zone of the galaxy ISM. A chemically homogeneity, across hundreds of parsecs, is observed in O/H. We take the oxygen abundance 12+log(O/H)=7.64 $\pm$ 0.06 derived from the PHL293B integrated spectrum as the representative metallicity for the galaxy. Our IFU data reveal for the first time that the nebular HeII4686 emission from PHL 293B is spatially extended and coincident with the ionizing stellar cluster, and allow us to compute its absolute HeII ionizing photon flux. Wolf-Rayet bumps are not detected excluding therefore Wolf-Rayet stars as the main HeII excitation source. The origin of the nebular HeII4686 is discussed.Comment: 14 pages, 9 Figures, 3 Tables; Accepted for publication in MNRA

Clinical Variables and Genetic Risk Factors Associated with the Acute Outcome of Ischemic Stroke : A Systematic Review

Stroke is a complex disease and one of the main causes of morbidity and mortality among the adult population. A huge variety of factors is known to influence patient outcome, including demographic variables, comorbidities or genetics. In this review, we expound what is known about the influence of clinical variables and related genetic risk factors on ischemic stroke outcome, focusing on acute and subacute outcome (within 24 to 48 hours after stroke and until day 10, respectively), as they are the first indicators of stroke damage. We searched the PubMed data base for articles that investigated the interaction between clinical variables or genetic factors and acute or subacute stroke outcome. A total of 61 studies were finally included in this review. Regarding the data collected, the variables consistently associated with acute stroke outcome are: glucose levels, blood pressure, presence of atrial fibrillation, prior statin treatment, stroke severity, type of acute treatment performed, severe neurological complications, leukocyte levels, and genetic risk factors. Further research and international efforts are required in this field, which should include genome-wide association studies

Clinical variables and genetic risk factors associated with the acute outcome of ischemic stroke : a systematic review

Stroke is a complex disease and one of the main causes of morbidity and mortality among the adult population. A huge variety of factors is known to influence patient outcome, including demographic variables, comorbidities or genetics. In this review, we expound what is known about the influence of clinical variables and related genetic risk factors on ischemic stroke outcome, focusing on acute and subacute outcome (within 24 to 48 hours after stroke and until day 10, respectively), as they are the first indicators of stroke damage. We searched the PubMed data base for articles that investigated the interaction between clinical variables or genetic factors and acute or subacute stroke outcome. A total of 61 studies were finally included in this review. Regarding the data collected, the variables consistently associated with acute stroke outcome are: glucose levels, blood pressure, presence of atrial fibrillation, prior statin treatment, stroke severity, type of acute treatment performed, severe neurological complications, leukocyte levels, and genetic risk factors. Further research and international efforts are required in this field, which should include genome-wide association studies.Publisher PDFPeer reviewe