Universal correlations along the BEC-BCS crossover

We show that the long-distance behavior of the two-body density correlation functions and the Cooper-pair probability density of a balanced mixture of a two-component Fermi gas at $T = 0$, is universal along the BEC-BCS crossover. Our result is demonstrated by numerically solving the mean-field BCS model for different finite short-range atomic interaction potentials. We find an analytic expression for the correlation length in terms of the chemical potential and the energy gap at zero momentum.Comment: 6 pages, 3 figure

Exploring the mediators that promote carotid body dysfunction in type 2 diabetes and obesity related syndromes

Carotid bodies (CBs) are peripheral chemoreceptors that sense changes in blood O2, CO2, and pH levels. Apart from ventilatory control, these organs are deeply involved in the homeostatic regulation of carbohydrates and lipid metabolism and inflammation. It has been described that CB dysfunction is involved in the genesis of metabolic diseases and that CB overactivation is present in animal models of metabolic disease and in prediabetes patients. Additionally, resection of the CB-sensitive nerve, the carotid sinus nerve (CSN), or CB ablation in animals prevents and reverses diet-induced insulin resistance and glucose intolerance as well as sympathoadrenal overactivity, meaning that the beneficial effects of decreasing CB activity on glucose homeostasis are modulated by target-related efferent sympathetic nerves, through a reflex initiated in the CBs. In agreement with our pre-clinical data, hyperbaric oxygen therapy, which reduces CB activity, improves glucose homeostasis in type 2 diabetes patients. Insulin, leptin, and pro-inflammatory cytokines activate the CB. In this manuscript, we review in a concise manner the putative pathways linking CB chemoreceptor deregulation with the pathogenesis of metabolic diseases and discuss and present new data that highlight the roles of hyperinsulinemia, hyperleptinemia, and chronic inflammation as major factors contributing to CB dysfunction in metabolic disorders.publishersversionpublishe

Advanced Patient-Centered Communication for Health Behavior Change: Motivational Interviewing Workshops for Medical Learners

Introduction: Medical settings are critical access points for behavior change counseling, and lifestyle behavior change is considered a key component of chronic disease management. The Association of American Medical Colleges recommends that future physicians be competent in shared decision making and patient-centered behavioral guidance to prevent illness and improve patient self-management of chronic disease. Motivational interviewing (MI) is a patient-centered, directive method of communication to enhance behavior change. Specific teachable strategies underlie the collaborative MI communication style that aims to reduce discord and build motivation for change. Methods: We present our three-session 12-hour MI curriculum as an advanced form of patient-centered communication. Each session includes presession assignment, large-group interactive lecture, and small-group activities for practice. An interdisciplinary team consisting of medical educators and health behavior change research-educators who are also members of the Motivational Interviewing Network of Trainers created the submission. The purpose of this resource is to provide medical educators with a short curriculum that incorporates materials and learning activities to promote skill in MI. Results: In addition to positive feedback from student evaluations including the areas of relevance to training and self-rated skills improvement, preliminary pre- and posttraining scores from the medical students show significant improvement in expression of empathy and the ratio of reflections to questions. Discussion: Implementation of the curriculum allows learners the opportunity to practice evidence-based communication that promotes intrinsic motivation for health behavior change in patients, a key treatment focus in chronic disease management

A strategy for implementing non-perturbative renormalisation of heavy-light four-quark operators in the static approximation

We discuss the renormalisation properties of the complete set of $\Delta B = 2$ four-quark operators with the heavy quark treated in the static approximation. We elucidate the role of heavy quark symmetry and other symmetry transformations in constraining their mixing under renormalisation. By employing the Schroedinger functional, a set of non-perturbative renormalisation conditions can be defined in terms of suitable correlation functions. As a first step in a fully non-perturbative determination of the scale-dependent renormalisation factors, we evaluate these conditions in lattice perturbation theory at one loop. Thereby we verify the expected mixing patterns and determine the anomalous dimensions of the operators at NLO in the Schroedinger functional scheme. Finally, by employing twisted-mass QCD it is shown how finite subtractions arising from explicit chiral symmetry breaking can be avoided completely.Comment: 41 pages, 6 figure

Involvement of the subthalamic nucleus in impulse control disorders associated with Parkinson’s disease

Behavioural abnormalities such as impulse control disorders may develop when patients with Parkinson’s disease receive dopaminergic therapy, although they can be controlled by deep brain stimulation of the subthalamic nucleus. We have recorded local field potentials in the subthalamic nucleus of 28 patients with surgically implanted subthalamic electrodes. According to the predominant clinical features of each patient, their Parkinson’s disease was associated with impulse control disorders (n = 10), dyskinesias (n = 9) or no dopaminergic mediated motor or behavioural complications (n = 9). Recordings were obtained during the OFF and ON dopaminergic states and the power spectrum of the subthalamic activity as well as the subthalamocortical coherence were analysed using Fourier transform-based techniques. The position of each electrode contact was determined in the postoperative magnetic resonance image to define the topography of the oscillatory activity recorded in each patient. In the OFF state, the three groups of patients had similar oscillatory activity. By contrast, in the ON state, the patients with impulse control disorders displayed theta-alpha (4–10 Hz) activity (mean peak: 6.71 Hz) that was generated 2–8mm below the intercommissural line. Similarly, the patients with dyskinesia showed theta-alpha activity that peaked at a higher frequency (mean: 8.38 Hz) and was generated 0–2mm below the intercommissural line. No such activity was detected in patients that displayed no dopaminergic side effects. Cortico-subthalamic coherence was more frequent in the impulsive patients in the 4–7.5 Hz range in scalp electrodes placed on the frontal regions anterior to the primary motor cortex, while in patients with dyskinesia it was in the 7.5–10 Hz range in the leads overlying the primary motor and supplementary motor area. Thus, dopaminergic side effects in Parkinson’s disease are associated with oscillatory activity in the theta-alpha band, but at different frequencies and with different topography for the motor (dyskinesias) and behavioural (abnormal impulsivity) manifestations. These findings suggest that the activity recorded in parkinsonian patients with impulse control disorders stems from the associative-limbic area (ventral subthalamic area), which is coherent with premotor frontal cortical activity. Conversely, in patients with L-dopa-induced dyskinesias such activity is recorded in the motor area (dorsal subthalamic area) and it is coherent with cortical motor activity. Consequently, the subthalamic nucleus appears to be implicated in the motor and behavioural complications associated with dopaminergic drugs in Parkinson’s disease, specifically engaging different anatomo-functional territories

The role of NADPH oxidase in carotid body arterial chemoreceptors

Producción CientíficaO2-sensing in the carotid body occurs in neuroectoderm-derived type I glomus cells where hypoxia elicits a complex chemotransduction cascade involving membrane depolarization, Ca2+ entry and the release of excitatory neurotransmitters. Efforts to understand the exquisite O2-sensitivity of these cells currently focus on the coupling between local PO2 and the open-closed state of K+-channels. Amongst multiple competing hypotheses is the notion that K+-channel activity is mediated by a phagocytic-like multisubunit enzyme, NADPH oxidase, which produces reactive oxygen species (ROS) in proportion to the prevailing PO2. In O2-sensitive cells of lung neuroepithelial bodies (NEB), multiple studies confirm that ROS levels decrease in hypoxia, and that EM and K+-channel activity are indeed controlled by ROS produced by NADPH oxidase. However, recent studies in our laboratories suggest that ROS generated by a non-phagocyte isoform of the oxidase are important contributors to chemotransduction, but that their role in type I cells differs fundamentally from the mechanism utilized by NEB chemoreceptors. Data indicate that in response to hypoxia, NADPH oxidase activity is increased in type I cells, and further, that increased ROS levels generated in response to low-O2 facilitate cell repolarization via specific subsets of K+-channels

High fat diet blunts the effects of leptin on ventilation and on carotid body activity

Funding : This study was supported by the Portuguese Foundation for Science and Technology grant PTDC/SAU-ORG/111417/2009 to S.C. and by Grants BFU2015-70616R from MINECO-FEDER, Spain. J.F.S. and B.F.M. are supported by PhD Grants from FCT, PD/BD/105890/2014 and PD/BD/128336/2017, respectively.Leptin plays a role in the control of breathing, acting mainly on central nervous structures. Leptin receptor is expressed in the carotid body (CB) and this finding has been associated with a putative physiological role of leptin in the regulation of CB function. Since, the CBs are implicated in energy metabolism herein we tested the effects of different concentrations of leptin administration on ventilatory parameters and on carotid sinus nerve (CSN) activity in control and high-fat (HF) diet fed rats, in order to clarify the role of leptin in ventilation control in metabolic disease states. We also investigated the expression of leptin receptors and the neurotransmitters involved in leptin signalling in the CBs. We found that in non-disease conditions, leptin increases minute ventilation both in basal and hypoxic conditions. However, in the HF model, the effect of leptin in ventilatory control is blunted. We also observed that HF rats display an increased frequency of CSN discharge in basal conditions that is not altered by leptin, in contrast to what is observed in control animals. Leptin did not modify intracellular Ca2+ in CB chemoreceptor cells, but it produced an increase in the release of adenosine from the whole CB. We conclude that CBs represent an important target for leptin signalling, not only to coordinate peripheral ventilatory chemoreflexive drive, but probably also to modulate metabolic variables. We also concluded that leptin signalling is mediated by adenosine release and that HF diets blunt leptin responses in the CB, compromising ventilatory adaptation. This article is protected by copyright. All rights reserved.publishersversionpublishe