Chickadees Faced with Unpredictable Food Increase Fat Reserves but Certain Components of Their Immune Function Decline

In winter, temperate resident birds are often faced with periodic low natural food availability. This reduction or unpredictability in resource availability might then have a negative impact on immune function, given that immune system support is highly resource dependent. We investigated the balance between energetic and immune management in captive black-capped chickadees (Poecile atricapilus) by manipulating the predictability of resources. The control group received food ad lib. every day, while the experimental group received a reduced amount of food on random days and food ad lib. on all other days. We measured two key metrics of energetic management (body and fat mass) as well as a suite of immune system components. Compared with control birds, experimental birds maintained significantly higher total body and fat mass, had lower acute phase protein concentrations, and had decreased body temperature and lost more body mass during the fever response following injection with lipopolysaccharides. Interestingly, birds in both groups had similar levels of complement lysis, delayed-type hypersensitivity response (phytohemagglutinin), and primary antibody production (keyhole limpet hemocyanin). This experiment demonstrates that black-capped chickadees strategically increase their fat mass in response to decreased food availability and that this might allow the birds to maintain most of the immune system unaltered, except some of the most costly immune components

Chickadees faced with unpredictable food increase fat reserves but certain components of their immune function decline

In winter, temperate resident birds are often faced with periodic low natural food availability. This reduction or unpredictability in resource availability might then have a negative impact on immune function, given that immune system support is highly resource dependent. We investigated the balance between energetic and immune management in captive black-capped chickadees (Poecile atricapilus) by manipulating the predictability of resources. The control group received food ad lib. every day, while the experimental group received a reduced amount of food on random days and food ad lib. on all other days. We measured two key metrics of energetic management (body and fat mass) as well as a suite of immune system components. Compared with control birds, experimental birds maintained significantly higher total body and fat mass, had lower acute phase protein concentrations, and had decreased body temperature and lost more body mass during the fever response following injection with lipopolysaccharides. Interestingly, birds in both groups had similar levels of complement lysis, delayed-type hypersensitivity response (phytohemagglutinin), and primary antibody production (keyhole limpet hemocyanin). This experiment demonstrates that black-capped chickadees strategically increase their fat mass in response to decreased food availability and that this might allow the birds to maintain most of the immune system unaltered, except some of the most costly immune components

Normal Aging Modulates the Neurotoxicity of Mutant Huntingtin

Aging likely plays a role in neurodegenerative disorders. In Huntington's disease (HD), a disorder caused by an abnormal expansion of a polyglutamine tract in the protein huntingtin (Htt), the role of aging is unclear. For a given tract length, the probability of disease onset increases with age. There are mainly two hypotheses that could explain adult onset in HD: Either mutant Htt progressively produces cumulative defects over time or “normal” aging renders neurons more vulnerable to mutant Htt toxicity. In the present study, we directly explored whether aging affected the toxicity of mutant Htt in vivo. We studied the impact of aging on the effects produced by overexpression of an N-terminal fragment of mutant Htt, of wild-type Htt or of a β-Galactosidase (β-Gal) reporter gene in the rat striatum. Stereotaxic injections of lentiviral vectors were performed simultaneously in young (3 week) and old (15 month) rats. Histological evaluation at different time points after infection demonstrated that the expression of mutant Htt led to pathological changes that were more severe in old rats, including an increase in the number of small Htt-containing aggregates in the neuropil, a greater loss of DARPP-32 immunoreactivity and striatal neurons as assessed by unbiased stereological counts

FEM-based Deformation Control for Dexterous Manipulation of 3D Soft Objects

International audienceIn this paper, a method for dexterous manipulation of 3D soft objects for real-time deformation control is presented, relying on Finite Element modelling. The goal is to generate proper forces on the fingertips of an anthropomor-phic device during in-hand manipulation to produce desired displacements of selected control points on the object. The desired motions of the fingers are computed in real-time as an inverse solution of a Finite Element Method (FEM), the forces applied by the fingertips at the contact points being modelled by Lagrange multipliers. The elasticity parameters of the model are preliminarly estimated using a vision system and a force sensor. Experimental results are shown with an underactuated anthropomorphic hand that performs a manipulation task on a soft cylindrical object

Loss of the thyroid hormone-binding protein Crym renders striatal neurons more vulnerable to mutant huntingtin in Huntington's disease

The mechanisms underlying preferential atrophy of the striatum in Huntington's disease (HD) are unknown. One hypothesis is that a set of gene products preferentially expressed in the striatum could determine the particular vulnerability of this brain region to mutant huntingtin (mHtt). Here, we studied the striatal protein µ-crystallin (Crym). Crym is the NADPH-dependent p38 cytosolic T3-binding protein (p38CTBP), a key regulator of thyroid hormone (TH) T3 (3,5,3′-triiodo-l-thyronine) transportation. It has been also recently identified as the enzyme that reduces the sulfur-containing cyclic ketimines, which are potential neurotransmitters. Here, we confirm the preferential expression of the Crym protein in the rodent and macaque striatum. Crym expression was found to be higher in the macaque caudate than in the putamen. Expression of Crym was reduced in the BACHD and Knock-in 140CAG mouse models of HD before onset of striatal atrophy. We show that overexpression of Crym in striatal medium-size spiny neurons using a lentiviral-based strategy in mice is neuroprotective against the neurotoxicity of an N-terminal fragment of mHtt in vivo. Thus, reduction of Crym expression in HD could render striatal neurons more susceptible to mHtt suggesting that Crym may be a key determinant of the vulnerability of the striatum. In addition our work points to Crym as a potential molecular link between striatal degeneration and the THs deregulation reported in HD patient

Encephalopathy induced by Alzheimer brain inoculation in a non-human primate.

Alzheimer's disease is characterized by cognitive alterations, cerebral atrophy and neuropathological lesions including neuronal loss, accumulation of misfolded and aggregated β-amyloid peptides (Aβ) and tau proteins. Iatrogenic induction of Aβ is suspected in patients exposed to pituitary-derived hormones, dural grafts, or surgical instruments, presumably contaminated with Aβ. Induction of Aβ and tau lesions has been demonstrated in transgenic mice after contamination with Alzheimer's disease brain homogenates, with very limited functional consequences. Unlike rodents, primates naturally express Aβ or tau under normal conditions and attempts to transmit Alzheimer pathology to primates have been made for decades. However, none of earlier studies performed any detailed functional assessments. For the first time we demonstrate long term memory and learning impairments in a non-human primate (Microcebus murinus) following intracerebral injections with Alzheimer human brain extracts. Animals inoculated with Alzheimer brain homogenates displayed progressive cognitive impairments (clinical tests assessing cognitive and motor functions), modifications of neuronal activity (detected by electroencephalography), widespread and progressive cerebral atrophy (in vivo MRI assessing cerebral volume loss using automated voxel-based analysis), neuronal loss in the hippocampus and entorhinal cortex (post mortem stereology). They displayed parenchymal and vascular Aβ depositions and tau lesions for some of them, in regions close to the inoculation sites. Although these lesions were sparse, they were never detected in control animals. Tau-positive animals had the lowest performances in a memory task and displayed the greatest neuronal loss. Our study is timely and important as it is the first one to highlight neuronal and clinical dysfunction following inoculation of Alzheimer's disease brain homogenates in a primate. Clinical signs in a chronic disease such as Alzheimer take a long time to be detectable. Documentation of clinical deterioration and/or dysfunction following intracerebral inoculations with Alzheimer human brain extracts could lead to important new insights about Alzheimer initiation processes

Nonprehensile Manipulation of Deformable Objects: Achievements and Perspectives from the RobDyMan Project

International audienceThe goal of this work is to disseminate the results achieved so far within the RODYMAN project related to planning and control strategies for robotic nonprehensile manipulation. The project aims at advancing the state of the art of nonprehensile dynamic manipulation of rigid and deformable objects to future enhance the possibility of employing robots in anthropic environments. The final demonstrator of the RODYMAN project will be an autonomous pizza maker. This article is a milestone to highlight the lessons learned so far and pave the way towards future research directions and critical discussions

16p11.2 600 kb Duplications confer risk for typical and atypical Rolandic epilepsy

Rolandic epilepsy (RE) is the most common idiopathic focal childhood epilepsy. Its molecular basis is largely unknown and a complex genetic etiology is assumed in the majority of affected individuals. The present study tested whether six large recurrent copy number variants at 1q21, 15q11.2, 15q13.3, 16p11.2, 16p13.11 and 22q11.2 previously associated with neurodevelopmental disorders also increase risk of RE. Our association analyses revealed a significant excess of the 600 kb genomic duplication at the 16p11.2 locus (chr16: 29.5-30.1 Mb) in 393 unrelated patients with typical (n = 339) and atypical (ARE; n = 54) RE compared with the prevalence in 65 046 European population controls (5/393 cases versus 32/65 046 controls; Fisher's exact test P = 2.83 × 10−6, odds ratio = 26.2, 95% confidence interval: 7.9-68.2). In contrast, the 16p11.2 duplication was not detected in 1738 European epilepsy patients with either temporal lobe epilepsy (n = 330) and genetic generalized epilepsies (n = 1408), suggesting a selective enrichment of the 16p11.2 duplication in idiopathic focal childhood epilepsies (Fisher's exact test P = 2.1 × 10−4). In a subsequent screen among children carrying the 16p11.2 600 kb rearrangement we identified three patients with RE-spectrum epilepsies in 117 duplication carriers (2.6%) but none in 202 carriers of the reciprocal deletion. Our results suggest that the 16p11.2 duplication represents a significant genetic risk factor for typical and atypical R