Traducción y adaptación transcultural al contexto español del marco teórico Person-Centred Practice Framework

Background. Person-centered care has become a key global approach that seeks to provide answers to all factors of the complex health care-related processes. This has led to the development of theoreti-cal frameworks that represent the components of person-centered care. The internationally recognized Person-Centred Practice Framework (PCPF) (McCormack and McCance) allows multidisciplinary teams to understand and operationalize the dimensions for the development of person-centered care. The aim of this study was to obtain the first Spanish version of the PCPF translated and adapted to the Spanish con-text. Methods. We translated the PCPF following the Translation and cul-tural adaptation process for Patient-Reported Outcomes (PRO) Measures guidelines. A consulting session with experts was part of the process and content validation on clarity and relevance for each domain was performed. Results. We encountered no significant difficulties to reach agree-ments on most of the terms except for Having a sympathetic presence. Not only was a complex term to translate but also to trans-culturally adapt. Regarding relevance and clarity, the content index by construct (I-CVI) and the global framework (S-CVI/Ave) were consistent with their original counterparts (>= 0.90). Conclusions. The adapted Spanish version is clear, significant, and conceptually equivalent to the original PCPF. It will allow a better com-prehension of the person-centered practice framework in the Spanish context and facilitate the implementation of this approach in clinical practices

Toll-like receptor signaling and stages of addiction

Athina Markou and her colleagues discovered persistent changes in adult behavior following adolescent exposure to ethanol or nicotine consistent with increased risk for developing addiction. Building on Dr. Markou's important work and that of others in the field, researchers at the Bowles Center for Alcohol Studies have found that persistent changes in behavior following adolescent stress or alcohol exposure may be linked to induction of immune signaling in brain. This study aims to illuminate the critical interrelationship of the innate immune system (e.g., toll-like receptors [TLRs], high-mobility group box 1 [HMGB1]) in the neurobiology of addiction. This study reviews the relevant research regarding the relationship between the innate immune system and addiction. Emerging evidence indicates that TLRs in brain, particularly those on microglia, respond to endogenous innate immune agonists such as HMGB1 and microRNAs (miRNAs). Multiple TLRs, HMGB1, and miRNAs are induced in the brain by stress, alcohol, and other drugs of abuse and are increased in the postmortem human alcoholic brain. Enhanced TLR-innate immune signaling in brain leads to epigenetic modifications, alterations in synaptic plasticity, and loss of neuronal cell populations, which contribute to cognitive and emotive dysfunctions. Addiction involves progressive stages of drug binges and intoxication, withdrawal-negative affect, and ultimately compulsive drug use and abuse. Toll-like receptor signaling within cortical-limbic circuits is modified by alcohol and stress in a manner consistent with promoting progression through the stages of addiction

One week high-fat diet alters MTR, T2 and ADC values in the mouse hypothalamus and reward centers

Trabajo presentado en el 37th Annual Meeting; European Society for Magnetic Resonance In Medicine and Biology (ESMRMB), celebrado en Rotterdam (Países Bajos) del 3 al 5 de octubre de 2019.[Purpose/Introduction]: Obesity development is linked to inflammation in the hypothalamus, the brain structure responsible for appetite regulation and energy homeostasis. Furthermore, appetite has in mammals a hedonic component, controlled by the reward centers, affected during inflammation1. In rodents, inflammation has been characterized, at a histological level, by the emergence of microgliosis and astrogliosis, events that can be detected before gain in body weight. Studies using Magnetic Resonance Imaging (MRI) have identified a rise in the transverse relaxation time (T2) –a surrogate marker of astrocytosis- in the hypothalamus of long-term highfat diet (HFD) mice and in obese patients. Nevertheless, no MRI hypothalamic inflammatory markers of the initial stages of obesity have yet been investigated, and the role of the reward centers remains to be determined. Therefore, the aim of this study was to assess the onset of obesity development in mice in vivo using MRI. We evaluated the longitudinal changes of T2, magnetization transfer ratios (MTR) and apparent diffusion coefficients (ADC) in mice during the initial stages of high-fat or standard diet consumption.[Subjects and Methods]: Two animal groups, fed with either standard food chow (n = 7) or with a 60% high-fat (butter-based) diet (n = 8) were investigated before diet diversification (T = 0) and on days 1, 7 and 14. Body weight and blood glucose levels were controlled at every time point. MRI were performed in a 7T magnet (Bruker Biospect). Briefly, the hypothalamus (Hyp), nucleus accumbens (ACB) and infralimbic area (ILA) were localized in a T2-image using an anatomical atlas, and T2 (50 images, TE: 12–600 ms,TR = 5000 ms), MTR (MT pulse on/off, TE/TR = 9.8/2500 ms) maps and DWI (9 b:200-2000 smm-2) were acquired (5 slices, 1.25 mm thickness, 0.16 9 0.16 mm2). Longitudinal changes of the fitted parameters were assessed statistically using SPSS and a generalized estimated equations model[Results]: Body weight and blood glucose levels increased significantly on HFD mice from days 1 and 7, respectively, and control animals increased only body weight after 14 days (Figure 1)

Feasibility of in vivo measurement of glucose metabolism in the mouse hypothalamus by ¹ H-[¹³ C] MRS at 14.1T.

Determine the feasibility of <sup>1</sup> H-[ <sup>13</sup> C] MRS in the mouse hypothalamus using a 14.1T magnet. We optimized the design of a <sup>1</sup> H-[ <sup>13</sup> C] surface coil to maximize the signal-to-noise ratio of <sup>1</sup> H-[ <sup>13</sup> C] MRS in the mouse hypothalamus. With enhanced signal, <sup>13</sup> C accumulation in glucose metabolites was measured in a 8.7 µL voxel in the hypothalamus of 5 healthy mice during the continuous administration of [1,6- <sup>13</sup> C <sub>2</sub> ]glucose. Accumulation of <sup>13</sup> C label in glucose C6 and lactate C3 was visible in the hypothalamus 11 min after glucose administration. The <sup>13</sup> C fractional enrichment (FE) curves of lactate C3, glutamate and glutamine C4, glutamate+glutamine C3 and C2, GABA C2, C3, and C4, and aspartate C3 were measured with a time resolution of 11 min over 190 min. FE time-courses and metabolic pool sizes were averaged to fit a novel one-compartment model of brain energy metabolism that incorporates the main features of the hypothalamus. Dynamic <sup>1</sup> H-[ <sup>13</sup> C] MRS is able to measure in vivo brain metabolism in small and deep areas of the mouse brain such as the hypothalamus, and it can be used to calculate metabolic fluxes, including glutamatergic and GABAergic metabolism as well as the contribution of metabolic sources other than glucose