Transgelin gene is frequently downregulated by promoter DNA hypermethylation in breast cancer

Tables not included in the main manuscript have been listed. Table S1. Number of probe sets affected by AZA treatment; Table S2. Comparison of significantly altered probe sets with the independent study GSE20713 Dataset; Table S3. Cancer vs. normal analysis of TAGLN mRNA in Oncomine database. (PDF 18 kb

Journée d'étude : L’usager, l’assistance et la question de la contrepartie

Journée en hommage à Robert Castel organisée par le LIRTES (UPEC) Le mardi 20 mai 2014 à Créteil Avec la participation de Colette Bec (« Usages politiques de l’assistance en démocratie ») et Christophe Trombert (« L’assistance aux pauvres valides : évolutions des contreparties »), membres du laboratoire LISE Bien que l’usager soit une catégorie relativement ancienne servant à désigner le rapport entre les personnes qui utilisent un service (logement, école, transport…) et les pouvoirs publics..

Additional file 3: of Transgelin gene is frequently downregulated by promoter DNA hypermethylation in breast cancer

Final gene lists altered upon AZA treatments only in breast cancer cell lines. Probe IDs, gene names, accession numbers and fold change ratios of the genes altered upon AZA treatment, in each breast cancer cell line at 1.5 fold and P < 0.05, and filtered as shown in Fig. 1A have been listed. (XLSX 387 kb

MCH neuron activity ıs sufficient for reward and reinforces feeding

Background: Melanin-concentrating hormone (MCH)-expressing neurons have been implicated in regulation of energy homeostasis and reward, yet the role of their electrical activity in short-term appetite and reward modulation has not been fully understood. Objectives: We investigated short-term behavioral and physiological effects of MCH neuron activity manipulations. Methods: We used optogenetic and chemogenetic approaches in Pmch-cre transgenic mice to acutely stimulate/inhibit MCH neuronal activity while probing feeding, locomotor activity, anxiety-like behaviors, glucose homeostasis, and reward. Results: MCH neuron activity is neither required nor sufficient for short-term appetite unless stimulation is temporally paired with consumption. MCH neuronal activation does not affect short-term locomotor activity, but inhibition improves glucose tolerance and is mildly anxiolytic. Finally, using two different operant tasks, we showed that activation of MCH neurons alone is sufficient to induce reward. Conclusions: Our results confirm diverse behavioral/physiological functions of MCH neurons and suggest a direct role in reward function.EMBO IG grant [2539]Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [214S0859999

AgRP neurons encode circadian feeding time

Food intake follows a predictable daily pattern and synchronizes metabolic rhythms. Neurons expressing agouti-related protein (AgRP) read out physiological energetic state and elicit feeding, but the regulation of these neurons across daily timescales is poorly understood. Using a combination of neuron dynamics measurements and timed optogenetic activation in mice, we show that daily AgRP-neuron activity was not fully consistent with existing models of homeostatic regulation. Instead of operating as a ‘deprivation counter’, AgRP-neuron activity primarily followed the circadian rest–activity cycle through a process that required an intact suprachiasmatic nucleus and synchronization by light. Imposing novel feeding patterns through time-restricted food access or periodic AgRP-neuron stimulation was sufficient to resynchronize the daily AgRP-neuron activity rhythm and drive anticipatory-like behavior through a process that required DMHPDYN neurons. These results indicate that AgRP neurons integrate time-of-day information of past feeding experience with current metabolic needs to predict circadian feeding time

Opioidergic signaling contributes to food-mediated suppression of AgRP neurons.

Opioids are generally known to promote hedonic food consumption. Although much of the existing evidence is primarily based on studies of the mesolimbic pathway, endogenous opioids and their receptors are widely expressed in hypothalamic appetite circuits as well; however, their role in homeostatic feeding remains unclear. Using a fluorescent opioid sensor, deltaLight, here we report that mediobasal hypothalamic opioid levels increase by feeding, which directly and indirectly inhibits agouti-related protein (AgRP)-expressing neurons through the μ-opioid receptor (MOR). AgRP-specific MOR expression increases by energy surfeit and contributes to opioid-induced suppression of appetite. Conversely, its antagonists diminish suppression of AgRP neuron activity by food and satiety hormones. Mice with AgRP neuron-specific ablation of MOR expression have increased fat preference without increased motivation. These results suggest that post-ingestion release of endogenous opioids contributes to AgRP neuron inhibition to shape food choice through MOR signaling

NTS catecholamine neurons mediate hypoglycemic hunger via medial hypothalamic feeding pathways

Glucose is the essential energy source for the brain, whose deficit, triggered by energy deprivation or therapeutic agents, can be fatal. Increased appetite is the key behavioral defense against hypoglycemia; however, the central pathways involved are not well understood. Here, we describe a glucoprivic feeding pathway by tyrosine hydroxylase (TH)-expressing neurons from nucleus of solitary tract (NTS), which project densely to the hypothalamus and elicit feeding through bidirectional adrenergic modulation of agouti-related peptide (AgRP)- and proopiomelanocortin (POMC)-expressing neurons. Acute chemogenetic inhibition of arcuate nucleus (ARC)-projecting NTSTH neurons or their target, AgRP neurons, impaired glucoprivic feeding induced by 2-Deoxy-D-glucose (2DG) injection. Neuroanatomical tracing results suggested that ARC-projecting orexigenic NTSTH neurons are largely distinct from neighboring catecholamine neurons projecting to parabrachial nucleus (PBN) that promotes satiety. Collectively, we describe a circuit organization in which an ascending pathway from brainstem stimulates appetite through key hunger neurons in the hypothalamus in response to hypoglycemia.EMBO IGFOEDR