Emotional feeding as interpersonal emotion regulation: A developmental risk factor for binge-eating behaviors

Emotional feeding is an interpersonal emotion regulation strategy wherein people provide food to others as a means of influencing the recipient's emotional response. Parental emotional feeding has been linked to higher levels of emotional eating in children and adolescents using cross-sectional, retrospective, and prospective designs; however, there is little research on emotional feeding as a developmental risk factor for emotional eating and binge-eating behaviors in adolescence and adulthood. This Idea Worth Researching article explores the rationale for studying emotional feeding as a lifespan construct and its potential implications for understanding eating disorder pathology. Specifically, it offers suggestions for examining emotional feeding as a predictor of emotional eating and binge-eating behavior across the lifespan, assessing potential intergenerational transmission pathways, and researching similarities in feeding styles and emotional eating across a variety of relationships beyond the parent–child dyad.     

Dynamic cerebral autoregulation to induced blood pressure changes in human experimental and clinical sepsis

Previous studies have demonstrated that dynamic cerebral autoregulation to spontaneous fluctuations in blood pressure is enhanced following lipopolysaccharide (LPS) infusion, a human experimental model of early sepsis, whereas by contrast it is impaired in patients with severe sepsis or septic shock. In this study, we hypothesized that this pattern of response would be identical during induced changes in blood pressure. Dynamic cerebral autoregulation was assessed in nine healthy volunteers and six septic patients. The healthy volunteers underwent a 4‐h intravenous infusion of LPS (total dose: 2 ng kg^?1). Mean arterial blood pressure (MAP, arterial transducer) and middle cerebral artery blood flow velocity (MCAv, transcranial Doppler ultrasound) were recorded continuously during thigh‐cuff deflation‐induced changes in MAP for the determination of a modified rate of regulation (RoR). This was performed before and after LPS infusion in healthy volunteers, and within 72 h following clinical diagnosis of sepsis in patients. In healthy volunteers, thigh‐cuff deflation caused a MAP reduction of 16 (13–20) % at baseline and 18 (16–20) % after LPS, while the MAP reduction was 12 (11–13) % in patients (P<0·05 versus volunteers at baseline; P<0·01 versus volunteers after LPS). The corresponding RoR values increased from 0·46 (0·31–0·49) s^?1 at baseline to 0·58 (0·36–0·74) s^?1 after LPS (P<0·05) in healthy volunteers, whereas they were similar to values observed in patients [0·43 (0·36–0·52) s^?1; P = 0·91 versus baseline; P = 0·14 versus LPS]. While our findings support the concept that dynamic cerebral autoregulation is enhanced during the very early stages of sepsis, they remain inconclusive with regard to more advanced stages of disease, because thigh‐cuff deflation failed to induce sufficient MAP reductions in patients.     

Atrial Capture Detection with Endocardial Electrodes

A new method of evoked response detection, previously demonstrated in the ventricle, has been studied in the atrium at the time of routine pacemaker implant in 16 patients. The atrial evoked response was readily detectable in all patients due to excellent recovery from poststimulus polarization. In six patients, as experimental threshold- tracking pacemaker was used to automatically verify atrial capture and to generate strength-duration curves. It is concluded that this pacing technique is both simple and reliable, and that automatic atrial threshold tracking is feasible.     

The in vivo effect of interleukin-1β on urea synthesis is mediated by glucocorticoids in rats

Abstract. Interleukin-1 β has been proposed as one mediator of parts of the catabolic response following surgery. However, it is not known whether such an effect is due to interleukin-1 β itself or the associated changes in glucocorticoids.
The effect of interleukin-1 β on urea synthesis was investigated in rats given a high (10 μg kg^-1) and a low dose (0·1 μg kg^-1) of recombinant interleukin-1 β (NOVO, Denmark) 3 h prior to determination of the rate of urea synthesis in vivo . Urea synthesis increased dose-dependently after the low dose from 4·0±0·3 (control) to 6·3±0·3 ( P <0·01), and after the high dose to 7·7±0·3 μmol (min·100 gBW)^-1 ( P <0·01). The blood concentration of amino acids fell during interleukin-1 β treatment, so the effect on urea synthesis was not due solely to increased proteolysis, but was exerted predominantly in the liver.
Pharmacological glucocorticoid receptor blockade (hormone analogue RU486, Roussel–Uclaf, Paris, France) given 1 h prior to the interleukin treatment, completely abolished the interleukin-1 β induced increases in urea synthesis. The study demonstrates that interleukin-1 β stimulates urea synthesis in vivo , and that the major part of the effect depends on glucocorticoid action.