Accessibiliser les pratiques de recherche sur le handicap : une approche par les droits humains.

INTRODUCTION: In this article, we offer an overview of the Capdroits participatory research approach, initially focusing on the controversy surrounding Article 12 of the International Convention of Persons with Disabilities, “Recognition of legal personality under conditions of equality.” Its objective is to encourage the participation of the people concerned by Article 12. It brings together academic researchers, experts in support relationships, and people directly concerned by impediment situations. PURPOSE OF THE STUDY: In this contribution, we present our participatory research approach, the methodology of “public problem-solving” and the ways in which it was deployed. We will show how productions and evaluations have been made accessible, while identifying the tensions at work. RESULTS: Two phases of research have been developed and deployed since 2015, based on an experimental “public problem-solving” methodology. Several collaborative productions have been developed, intended for various types of reception and made possible thanks to accessibility practices. They nevertheless highlight the tensions produced in the participatory processes. CONCLUSIONS: The epistemology that we have been collectively developing since 2015 radically aims to reduce social and cognitive inequalities by promoting experiential knowledge while perpetuating inequalities. Our ability to dialogue [14] is the basis for co-constructing a radical epistemology, which, while imperfect, is profoundly purposeful.

Potential Consequences of the Red Blood Cell Storage Lesion on Cardiac Electrophysiology.

Background The red blood cell (RBC) storage lesion is a series of morphological, functional, and metabolic changes that RBCs undergo following collection, processing, and refrigerated storage for clinical use. Since the biochemical attributes of the RBC unit shifts with time, transfusion of older blood products may contribute to cardiac complications, including hyperkalemia and cardiac arrest. We measured the direct effect of storage age on cardiac electrophysiology and compared it with hyperkalemia, a prominent biomarker of storage lesion severity. Methods and Results Donor RBCs were processed using standard blood-banking techniques. The supernatant was collected from RBC units, 7 to 50 days after donor collection, for evaluation using Langendorff-heart preparations (rat) or human induced pluripotent stem cell-derived cardiomyocytes. Cardiac parameters remained stable following exposure to "fresh" supernatant from red blood cell units (day 7: 5.8±0.2 mM K+), but older blood products (day 40: 9.3±0.3 mM K+) caused bradycardia (baseline: 279±5 versus day 40: 216±18 beats per minute), delayed sinus node recovery (baseline: 243±8 versus day 40: 354±23 ms), and increased the effective refractory period of the atrioventricular node (baseline: 77±2 versus day 40: 93±7 ms) and ventricle (baseline: 50±3 versus day 40: 98±10 ms) in perfused hearts. Beating rate was also slowed in human induced pluripotent stem cell-derived cardiomyocytes after exposure to older supernatant from red blood cell units (-75±9%, day 40 versus control). Similar effects on automaticity and electrical conduction were observed with hyperkalemia (10-12 mM K+). Conclusions This is the first study to demonstrate that "older" blood products directly impact cardiac electrophysiology, using experimental models. These effects are likely caused by biochemical alterations in the supernatant from red blood cell units that occur over time, including, but not limited to hyperkalemia. Patients receiving large volume and/or rapid transfusions may be sensitive to these effects.

7q21.11 Microdeletion in a Neonate With Goldenhar Syndrome: Case Report and a Literature Review.

The oculoauriculovertebral spectrum or Goldenhar syndrome is characterized by varying degrees of prevalently unilateral underdevelopment of the craniofacial structures (orbit, ear, and mandible) in association with vertebral, cardiac, renal, and central nervous system defects. We report on a term neonate with a partial monosomy 7q21.11 with marked hemifacial microsomia, facial clefting, and spinal anomaly. The estimated size of the monosomic region of 7q21.11 was approximately 55 kilobases. This is the first report of a patient with partial monosomy 7q21.11 associated with oculoauriculovertebral spectrum.

2q31.1 microdeletion syndrome: case report and literature review.

We describe a preterm neonate with bilateral coloboma of the iris, upper and lower limb malformations including rocker bottom feet, camptodactyly, and clinodactyly together with microcephaly and small for gestational age whom cytogenetic diagnosis using SNP microarray detected an interstitial deletion of chromosome 2 between 2q31.1 and 33.1.

BDNF: a missing link between sympathetic dysfunction and inflammatory disease?

Nerve growth factor (NGF) plays a role in sympathetic neuron integrity and survival. Brain-derived neurotrophic factor (BDNF) also has trophic effects on sympathetic neurons. We report here the serendipitous finding that co-treatment of hippocampus with BDNF and the NGF antagonist TrkA-Fc leads to perivascular inflammation and marked vasoconstriction. This effect is not observed with either reagent alone or in combination with other control proteins. Because NGF supports sympathetic neuron health, we tested the hypothesis that BDNF combined with sympathetic compromise caused this effect. Superior cervical ganglia were removed bilaterally with concurrent BDNF infusion into hippocampus. Perivascular inflammation was observed at 3 days, but not 12 days post treatment, when sympathetic terminals had receded, suggesting that the presence of these terminals was necessary for inflammation. Since sympathetic dysfunction may lead to compensatory overactivity of norepinephrine (NE) signaling, we co-infused BDNF with NE in the hippocampus and observed perivascular inflammation. In humans, sympathetic overactivity has been reported in a variety of vascular diseases. Some of these diseases, e.g. primary Raynaud's, are not accompanied by serious inflammatory disease whereas others, such as scleroderma and systemic lupus, are. We speculate that BDNF may contribute to the transformation of sympathetic dysfunction to inflammatory disease.