The antihypertensive and antihypertrophic effect of lycopene is not affected by and is independent of age

Hypertension of SHR appears at an early age and progressively increases. This study aimed to evaluate the effect of lycopene in SHR with mild hypertension (young rats) or with high level of hypertension (adult rats). Four-weeks treatment with 10 mg/kg/day of lycopene progressively decreased blood pressure in young (from 144 ± 2 to 119 ± 3 mmHg) and adult (from 177 ± 5 to 159 ± 7 mmHg) SHR. Heart and renal hypertrophy and fibrosis were increased in adult compared to young SHR and lycopene, regardless of the age of the rats, improved the injury in both organs. Although aging induced morphological and functional alterations in the aorta, the treatment was only effective in preventing the former. Lycopene helped to improve all the parameters linked to oxidative stress determined in this study. In conclusion, lycopene treatment improved the age-associated harmful changes in hypertension, cardiovascular and renal remodelling, and indicators of oxidant-antioxidant systems in both young and adult SHR.This work was financed by the University of Salamanca (Spain). Pedro Ferreira Santos was the recipient of a fellowship funded by a project Art.83/LOU of University of Salamanca. Lycopene was kindly supplied by DSM NUTRITIONAL PRODUCTSinfo:eu-repo/semantics/publishedVersio

Influence of seed layer thickness on properties of electrodeposited ZnO nanostructured films

[EN] The quality and properties of electrodeposited nanostructured ZnO films are improved when they are deposited on a crystal lattice-matching substrate. To this end, a highly conductive indium tin oxide substrate is covered with an interlayer of ZnO using direct-current magnetron sputtering. In this manuscript, we describe the effect of this interlayer on the morphological and optical properties of several nanostructured ZnO films grown by different electrodeposition methods. The thickness of the ZnO interlayer was varied starting from ultrathin layers of 10 nm all the way up to 230 nm as determined by ellipsonnetry. The structural and optical properties of the nanostructured ZnO films deposited on top of these interlayers were characterized using field emission scanning electron microscopy (FESEM), atomic force microscopy and UV-visible spectroscopy. Optimum properties of the nanostructured ZnO films for application in thin-film optoelectronic devices are obtained when the ZnO interlayer has a thickness of approximately 45 nm. This is the case for all the electrodeposition methods used in this work.Reyes Tolosa, MD.; Alajami, M.; Montero Reguera, ÁE.; Damonte, L.; Hernández Fenollosa, MDLÁ. (2019). Influence of seed layer thickness on properties of electrodeposited ZnO nanostructured films. SN Applied Sciences. 1(10):1-9. https://doi.org/10.1007/s42452-019-1293-719110Marotti RE, Giorgi P, Machado G, Dalchiele EA (2006) Crystallite size dependence of band gap energy for electrodeposited ZnO grown at different temperatures. Sol Energy Mater Sol Cells 90:2356–2361Marotti RE, Guerra DN, Bello C, Machado G (2004) Bandgap energy tuning of electrochemically grown ZnO thin films by thickness and electrodeposition potential. 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Immunosuppression-independent role of regulatory T cells against hypertension-driven renal dysfunctions

Hypertension-associated cardiorenal diseases represent one of the heaviest burdens for current health systems. In addition to hemodynamic damage, recent results have revealed that hematopoietic cells contribute to the development of these diseases by generating proinflammatory and profibrotic environments in the heart and kidney. However, the cell subtypes involved remain poorly characterized. Here we report that CD39+ regulatory T (TREG) cells utilize an immunosuppression-independent mechanism to counteract renal and possibly cardiac damage during angiotensin II (AngII)-dependent hypertension. This mechanism relies on the direct apoptosis of tissue-resident neutrophils by the ecto-ATP diphosphohydrolase activity of CD39. In agreement with this, experimental and genetic alterations in TREG/TH cell ratios have a direct impact on tissue-resident neutrophil numbers, cardiomyocyte hypertrophy, cardiorenal fibrosis, and, to a lesser extent, arterial pressure elevation during AngII-driven hypertension. These results indicate that TREG cells constitute a first protective barrier against hypertension-driven tissue fibrosis and, in addition, suggest new therapeutic avenues to prevent hypertension-linked cardiorenal diseases.This work has been supported by grants from the Castilla-León Autonomous Government (CSI101U13), the Spanish Ministry of Economy and Competitiveness (SAF2012-31371, RD12/0036/0002), Worldwide Cancer Research, the Solórzano Foundation, and the Ramón Areces Foundation to X.R.B. P.M. is funded by the Spanish Ministry of Economy and Competitiveness (SAF2011-27330). S.F., M.M.-M., J.R.-V., and A.M.-M. were supported by the Spanish Ministry of Economy and Competitiveness through BES-2010-031386, CSIC JAE-Doc, Juan de la Cierva, and BES-2009-016103 contracts, respectively. Spanish government-sponsored funding to X.R.B. is partially supported by the European Regional Development Fund.Peer Reviewe

The sigma-1 receptor curtails endogenous opioid analgesia during sensitization of TRPV1 nociceptors

Background and Purpose: Peripheral sensitization contributes to pathological pain. While prostaglandin E2 (PGE2) and nerve growth factor (NGF) sensitize peptidergic C-nociceptors (TRPV1+), glial cell line-derived neurotrophic factor (GDNF) sensitizes non-peptidergic C-neurons (IB4+). Sigma-1 receptor (σ1R) is a Ca2+-sensing chaperone known to modulate analgesia induced by opioid drugs. This receptor binds both to TRPV1 and the µ-opioid receptor (MOPr), although the functional repercussions of these physical interactions in peripheral sensitization are unknown. Experimental Approach: We tested the effect of sigma-1 antagonism on PGE2-, NGF- and GDNF-induced mechanical and heat hyperalgesia in mice. We used immunohistochemistry to determine the presence of endomorphin-2, an endogenous MOPr agonist, on dorsal root ganglion (DRG) neurons. Recombinant proteins were used to study the interactions between σ1R, MOPr and TRPV1. We used calcium imaging to study the effects of sigma-1 antagonism on PGE2-induced sensitization of TRPV1+ nociceptors. Key Results: σ1R antagonists reversed PGE2- and NGF-induced hyperalgesia, but not GDNF-induced hyperalgesia. Endomorphin-2 was detected on TRPV1+ but not on IB4+ neurons. Peripheral opioid receptor antagonism by naloxone methiodide or administration of an anti-endomorphin-2 antibody to a sensitized paw, reversed the antihyperalgesia induced by sigma-1 antagonists. Sigma-1 antagonism transfers σ1R from TRPV1 to MOPr, suggesting that σ1R participate in TRPV1-MOPr crosstalk. Moreover, σ1R antagonism reversed, in a naloxone-sensitive manner, PGE2-induced sensitization of DRG neurons to the calcium flux elicited by capsaicin, the prototypic TRPV1 agonist. Conclusion and Implications: σ1R antagonism harnesses endogenous opioids produced by TRPV1+ neurons to reduce hyperalgesia by increasing MOPr activity

Diverse Large HIV-1 Non-subtype B Clusters Are Spreading Among Men Who Have Sex With Men in Spain

In Western Europe, the HIV-1 epidemic among men who have sex with men (MSM) is dominated by subtype B. However, recently, other genetic forms have been reported to circulate in this population, as evidenced by their grouping in clusters predominantly comprising European individuals. Here we describe four large HIV-1 non-subtype B clusters spreading among MSM in Spain. Samples were collected in 9 regions. A pol fragment was amplified from plasma RNA or blood-extracted DNA. Phylogenetic analyses were performed via maximum likelihood, including database sequences of the same genetic forms as the identified clusters. Times and locations of the most recent common ancestors (MRCA) of clusters were estimated with a Bayesian method. Five large non-subtype B clusters associated with MSM were identified. The largest one, of F1 subtype, was reported previously. The other four were of CRF02_AG (CRF02_1; n = 115) and subtypes A1 (A1_1; n = 66), F1 (F1_3; n = 36), and C (C_7; n = 17). Most individuals belonging to them had been diagnosed of HIV-1 infection in the last 10 years. Each cluster comprised viruses from 3 to 8 Spanish regions and also comprised or was related to viruses from other countries: CRF02_1 comprised a Japanese subcluster and viruses from 8 other countries from Western Europe, Asia, and South America; A1_1 comprised viruses from Portugal, United Kingom, and United States, and was related to the A1 strain circulating in Greece, Albania and Cyprus; F1_3 was related to viruses from Romania; and C_7 comprised viruses from Portugal and was related to a virus from Mozambique. A subcluster within CRF02_1 was associated with heterosexual transmission. Near full-length genomes of each cluster were of uniform genetic form. Times of MRCAs of CRF02_1, A1_1, F1_3, and C_7 were estimated around 1986, 1989, 2013, and 1983, respectively. MRCA locations for CRF02_1 and A1_1 were uncertain (however initial expansions in Spain in Madrid and Vigo, respectively, were estimated) and were most probable in Bilbao, Spain, for F1_3 and Portugal for C_7. These results show that the HIV-1 epidemic among MSM in Spain is becoming increasingly diverse through the expansion of diverse non-subtype B clusters, comprising or related to viruses circulating in other countries.This work was funded through Acción Estratégica en Salud Intramural (AESI), Instituto de Salud Carlos III, project “Estudios sobre vigilancia epidemiológica molecular del VIH-1 en España,” PI16CIII/00033; Red de Investigación en SIDA (RIS), Instituto de Salud Carlos III, Subdirección General de Evaluación y Fondo Europeo de Desarrollo Regional (FEDER), Plan Nacional I+D+I, project RD16ISCIII/0002/0004; scientific agreements with Consellería de Sanidade, Government of Galicia (MVI 1004/16) and Osakidetza-Servicio Vasco de Salud, Government of Basque Country (MVI 1001/16); European Research Infrastructures for Poverty Related Diseases (EURIPRED). Seventh Framework Program: FP7-Capacities-infrastructures-2012-1, grant agreement 312661; and Dirección General de Farmacia, Ministerio de Sanidad, Servicios Sociales e Igualdad, Government of Spain (grant EC11-272).S