La recherche-intervention pour une transition vers le développement durable

La transition vers le développement durable est ici abordée par la démarche de la recherche-intervention. L’implication des chercheurs dans une action collective les oblige à construire de nouveaux rapports entre recherche et acteurs de manière à rendre la première pertinente par rapport aux enjeux identifiés. La démarche étudiée dans cet article, le cas d’une filière bovine bio, comporte une étape d’identification des préoccupations et des points de vue. Leur analyse conduit, d’un côté à une proposition d’action qui reconfigure les relations et les stabilise via des objets intermédiaires, et de l’autre à une proposition de recherches qui peuvent répondre aux défis de l’action en cours. Ces recherches relèvent de différents modèles selon la manière dont les acteurs et les objets peuvent y être associés. Leurs résultats alimentent l’action en cours et débouchent sur un nouveau référentiel de filière.The transition towards sustainable development is tackled by the “deliberative research” approach. The involvement of researchers in the collective action, obliges them to build new relations between research and actors, making the research relevant regarding the identified stakes. The approach – in this case of an organic beef food chain – starts by an identification step of concerns and viewpoints. The analysis leads on one hand to a proposal of action, which reconfigures the relations and stabilizes intermediary objects and on the other hand to research proposals which are intended to give answers to issues related to the action. These researches are related to different models according the way they associate actors and objects. Their outcomes feed the running action and open to a new food chain «référentiel» (frame of reference)

POLG2 deficiency causes adult-onset syndromic sensory neuropathy, ataxia and parkinsonism

Objective: Mitochondrial dysfunction plays a key role in the pathophysiology of neurodegenerative disorders such as ataxia and Parkinson's disease. We describe an extended Belgian pedigree where seven individuals presented with adult-onset cerebellar ataxia, axonal peripheral ataxic neuropathy, and tremor, in variable combination with parkinsonism, seizures, cognitive decline, and ophthalmoplegia. We sought to identify the underlying molecular etiology and characterize the mitochondrial pathophysiology of this neurological syndrome. Methods: Clinical, neurophysiological, and neuroradiological evaluations were conducted. Patient muscle and cultured fibroblasts underwent extensive analyses to assess mitochondrial function. Genetic studies including genome-wide sequencing were conducted. Results: Hallmarks of mitochondrial dysfunction were present in patients' tissues including ultrastructural anomalies of mitochondria, mosaic cytochrome c oxidase deficiency, and multiple mtDNA deletions. We identified a splice acceptor variant in POLG2, c.970-1G>C, segregating with disease in this family and associated with a concomitant decrease in levels of POLG2 protein in patient cells. Interpretation: This work extends the clinical spectrum of POLG2 deficiency to include an overwhelming, adult-onset neurological syndrome that includes cerebellar syndrome, peripheral neuropathy, tremor, and parkinsonism. We therefore suggest to include POLG2 sequencing in the evaluation of ataxia and sensory neuropathy in adults, especially when it is accompanied by tremor or parkinsonism with white matter disease. The demonstration that deletions of mtDNA resulting from autosomal-dominant POLG2 variant lead to a monogenic neurodegenerative multicomponent syndrome provides further evidence for a major role of mitochondrial dysfunction in the pathomechanism of nonsyndromic forms of the component neurodegenerative disorders

Circadian function in patients with advanced non-small-cell lung cancer

This study aimed to evaluate whether patients with advanced non-small-cell lung cancer experience disrupted rest–activity daily rhythms, poor sleep quality, weakness, and maintain attributes that are linked to circadian function such as fatigue. This report describes the rest–activity patterns of 33 non-small-cell lung cancer patients who participated in a randomised clinical trial evaluating the benefits of melatonin. Data are reported on circadian function, health-related quality of life (QoL), subjective sleep quality, and anxiety/depression levels prior to randomisation and treatment. Actigraphy data, an objective measure of circadian function, demonstrated that patients' rest–activity circadian function differs significantly from control subjects. Our patients reported poor sleep quality and high levels of fatigue. Ferrans and Powers QoL Index instrument found a high level of dissatisfaction with health-related QoL. Data from the European Organization for Research and Treatment for Cancer reported poor capacity to fulfil the activities of daily living. Patients studied in the hospital during or near chemotherapy had significantly more abnormal circadian function than those studied in the ambulatory setting. Our data indicate that measurement of circadian sleep/activity dynamics should be accomplished in the outpatient/home setting for a minimum of 4–7 circadian cycles to assure that they are most representative of the patients' true condition. We conclude that the daily sleep/activity patterns of patients with advanced lung cancer are disturbed. These are accompanied by marked disruption of QoL and function. These data argue for investigating how much of this poor functioning and QoL are actually caused by this circadian disruption, and, whether behavioural, light-based, and or pharmacologic strategies to correct the circadian/sleep activity patterns can improve function and QoL

Abdominal wall paresis as a complication of laparoscopic surgery

Purpose: Abdominal wall nerve injury as a result of trocar placement for laparoscopic surgery is rare. We intend to discuss causes of abdominal wall paresis as well as relevant anatomy. Methods: A review of the nerve supply of the abdominal wall is illustrated with a rare case of a patient presenting with paresis of the internal oblique muscle due to a trocar lesion of the right iliohypogastric nerve after laparoscopic appendectomy. Results: Trocar placement in the upper lateral abdomen can damage the subcostal nerve (Th12), caudal intercostal nerves (Th7-11) and ventral rami of the thoracic nerves (Th7-12). Trocar placement in the lower abdomen can damage the ilioinguinal (L1 or L2) and iliohypogastric nerves (Th12-L1). Pareses of abdominal muscles due to trocar placement are rare due to overlap in innervation and relatively small sizes of trocar incisions. Conclusion: Knowledge of the anatomy of the abdominal wall is mandatory in order to avoid the injury of important structures during trocar placement

Peripheral electrical nerve stimulation and rest-activity rhythm in Alzheimer's disease

Rest-activity rhythm disruption is a prominent clinical feature of Alzheimer's disease (AD). The origin of the altered rest-activity rhythm is believed to be degeneration of the suprachiasmatic nucleus (SCN). In accordance with the 'use it or lose it' hypothesis of Swaab [Neurobiol Aging 1991, 12: 317-324] stimulation of the SCN may prevent age-related loss of neurons and might reactivate nerve cells that are inactive but not lost. Previous studies with relatively small sample sizes have demonstrated positive effects of peripheral electrical nerve stimulation on the rest-activity rhythm in AD patients. The present randomized, placebo-controlled, parallel-group study was meant to replicate prior findings of electrical stimulation in AD in a substantially larger group of AD patients. The experimental group (n = 31) received peripheral electrical nerve stimulation and the placebo group (n = 31) received sham stimulation. Effects of the intervention on the rest-activity rhythm were assessed by using wrist-worn actigraphs. Near-significant findings on the rest-activity rhythm partially support the hypothesis that neuronal stimulation enhances the rest-activity rhythm in AD patients. Interestingly, post-hoc analyses revealed significant treatment effects in a group of patients who were not using acetylcholinesterase inhibitors concomitantly. We conclude that more research is needed before firm general conclusions about the effectiveness of electrical stimulation as a symptomatic treatment in AD can be drawn. In addition, the present post-hoc findings indicate that future studies on non-pharmacological interventions should take medication use into account

Circadian Phase Resetting via Single and Multiple Control Targets

Circadian entrainment is necessary for rhythmic physiological functions to be appropriately timed over the 24-hour day. Disruption of circadian rhythms has been associated with sleep and neuro-behavioral impairments as well as cancer. To date, light is widely accepted to be the most powerful circadian synchronizer, motivating its use as a key control input for phase resetting. Through sensitivity analysis, we identify additional control targets whose individual and simultaneous manipulation (via a model predictive control algorithm) out-perform the open-loop light-based phase recovery dynamics by nearly 3-fold. We further demonstrate the robustness of phase resetting by synchronizing short- and long-period mutant phenotypes to the 24-hour environment; the control algorithm is robust in the presence of model mismatch. These studies prove the efficacy and immediate application of model predictive control in experimental studies and medicine. In particular, maintaining proper circadian regulation may significantly decrease the chance of acquiring chronic illness