How do African grey parrots (Psittacus erithacus) perform on a delay of gratification task?

Humans and other animals often find it difficult to choose a delayed reward over an immediate one, even when the delay leads to increased pay-offs. Using a visible incremental reward procedure, we tested the ability of three grey parrots to maintain delay of gratification for an increasingly valuable food pay-off. Up to 5 sunflower seeds were placed within the parrot’s reach, one at a time, at a rate of 1 seed per second. When the parrot took a seed the trial was ended and the birds consumed the accumulated seeds. Parrots were first tested in daily sessions of 10 trials and then with single daily trials. For multiple trial sessions, all three parrots showed some limited improvement across 30 sessions. For single trial sessions, only one parrot showed any increase in seed acquisition across trials. This parrot was also able to consistently obtain two or more seeds per trial (across both multiple and single trial conditions) but was unable to able to wait 5 seconds to obtain the maximum number of seeds. This parrot was also tested on a slower rate of seed presentation, and this significantly reduced her mean seed acquisition in both multiple and single trial conditions, suggesting that both value of reward available and delay duration impact upon self-control. Further manipulation of both the visibility and proximity of seeds during delay maintenance had little impact upon tolerance of delays for both parrots tested in this condition. This task demanded not just a choice of delayed reward but the maintenance of delayed gratification and was clearly difficult for the parrots to learn; additional training or alternative paradigms are required to better understand the capacity for self-control in this species

Increased Infarct Wall Thickness by a Bio-Inert Material Is Insufficient to Prevent Negative Left Ventricular Remodeling after Myocardial Infarction

Several injectable materials have been shown to preserve or improve cardiac function as well as prevent or slow left ventricular (LV) remodeling post-myocardial infarction (MI). However, it is unclear as to whether it is the structural support or the bioactivity of these polymers that lead to beneficial effects. Herein, we examine how passive structural enhancement of the LV wall by an increase in wall thickness affects cardiac function post-MI using a bio-inert, non-degradable synthetic polymer in an effort to better understand the mechanisms by which injectable materials affect LV remodeling.Poly(ethylene glycol) (PEG) gels of storage modulus G' = 0.5±0.1 kPa were injected and polymerized in situ one week after total occlusion of the left coronary artery in female Sprague Dawley rats. The animals were imaged using magnetic resonance imaging (MRI) at 7±1 day(s) post-MI as a baseline and again post-injection 49±4 days after MI. Infarct wall thickness was statistically increased in PEG gel injected vs. control animals (p<0.01). However, animals in the polymer and control groups showed decreases in cardiac function in terms of end diastolic volume, end systolic volume and ejection fraction compared to baseline (p<0.01). The cellular response to injection was also similar in both groups.The results of this study demonstrate that passive structural reinforcement alone was insufficient to prevent post-MI remodeling, suggesting that bioactivity and/or cell infiltration due to degradation of injectable materials are likely playing a key role in the preservation of cardiac function, thus providing a deeper understanding of the influencing properties of biomaterials necessary to prevent post-MI negative remodeling

Short-term Mechanical Unloading and Reverse Remodeling of Failing Hearts in Children.

BACKGROUND: Mechanical support using a left ventricular assist device (LVAD) can lead to functional recovery of the myocardium in patients with end-stage heart failure (HF). Molecular remodeling, cytoskeletal disruption, and apoptosis activation are associated with abnormal gene expression in the failing ventricular myocardium of HF subjects and can normalize in response to medium- and long-term mechanical unloading in adults. However, there is little knowledge of the changes in gene expression after short-term mechanical support in children with HF. METHODS: We evaluated left ventricular biopsies from 4 children with HF. The children had implantation of a continuous- or a pulsatile-flow LVAD for 8 to 16 days before undergoing heart transplantation. At the time of LVAD insertion and removal, we performed quantitative real-time polymerase chain reaction (QPCR) to study the expression of 326 genes encoding for structural, transcriptional, and signaling pathways proteins, and immunoblot analysis on dystrophin and apoptotic factors. RESULTS: Short-term LVAD therapy significantly decreased brain natriuretic peptide (BNP) levels from pre-LVAD (3,584.5 378.3 pg/ml [95% CI]) to post-LVAD (447.5 52.7 pg/ml [95% CI]) in 2 patients in whom comparative BNP measurements were available. In addition, short-term LVAD therapy reduced HF and apoptosis markers, whereas it upregulated structural proteins, including dystrophin, as well as pro-hypertrophic and pro-inotropic markers. Furthermore, LVAD therapy normalized expression of genes involved in calcium homeostasis, cell growth, and differentiation. CONCLUSIONS: Our pilot study suggests that even short-term LVAD therapy in children with severe HF can reverse molecular remodeling. This favorable effect should be taken into consideration in eligible children with significant ventricular dysfunction