Aggressive behaviors are widespread among animals and are critical in the competition for resources.  https://www.selleckchem.com/products/dinaciclib-sch727965.html  The physiological mechanisms underlying aggression have mostly been examined in breeding males, in which gonadal androgens, acting in part through their aromatization to estrogens, have a key role. There are two alternative models that contribute to further understanding hormonal mechanisms underlying aggression aggression displayed in the non-breeding season, when gonadal steroids are low, and female aggression. In this study we approach, for the first time, the modulatory role of estrogens and androgens upon non-breeding aggression in a wild female teleost fish. We characterized female aggression in the weakly electric fish Gymnotus omarorum and carried out acute treatments 1 h prior to agonistic encounters in dyads treated with either an aromatase inhibitor or an antagonist of androgen receptors. Anti-androgen treatment had no effect on behavior whereas acute aromatase inhibition caused a strong distortion of aggressive behavior. Territorial non-breeding aggression was robust and depended on rapid estrogen actions to maintain high levels of aggression, and ultimately reach conflict resolution from which dominant/subordinate status emerged. Our results, taken together with our own reports in males and the contributions from non-breeding aggression in bird and mammal models, suggest a common strategy involving fast-acting estrogens in the control of this behavior across species. In addition, further analysis of female non-breeding aggression may shed light on potential sexual differences in the fine tuning of social behaviors. We have recently demonstrated that N(6)-cyclopentyladenosine (CPA), an adenosine A1 receptor agonist, acts centrally to induce a visceral antinociception. Since serotonin (5-HT), cannabinoid (CB), dopamine or opioid signaling in the central nervous system is involved in the regulation of visceral sensation, we made a hypothesis that the signaling may play a role in the CPA-induced visceral antinociception. Visceral sensation was evaluated by colonic distension-induced abdominal withdrawal reflex (AWR) in conscious rats. Subcutaneously administered CPA significantly increased the threshold of colonic distension-induced AWR. Intracisternal injection of either 5-HT1A or 5-HT2A receptor antagonist blocked the CPA-induced visceral antinociception while 5-HT1B antagonist did not block the CPA-induced visceral antinociception. Subcutaneous injection of dopamine D1 receptor antagonist, CB1 receptor antagonist or naloxone significantly blocked the CPA-induced visceral antinociception while neither subcutaneous injection of dopamine D2 receptor antagonist nor CB2 receptor antagonist blocked the CPA-induced anti-pain action. These results suggest that 5-HT1A, 5-HT2A, dopamine D1, CB1 receptors and the opioid system in the CNS may specifically mediate the CPA-induced visceral antinociception. These findings may help in understanding the physiological relevance of central adenosine with special reference to the pathophysiology of altered visceral sensation especially in irritable bowel syndrome. A new coronavirus (SARS-CoV-2) highlighted at the end of 2019 in China is spreading across all continents. Most often at the origin of a mild infectious syndrome, associating mild symptoms (fever, cough, myalgia, headache and possible digestive disorders) to different degrees, SARS-Covid-2 can cause serious pulmonary pathologies and sometimes death. Data on the consequences during pregnancy are limited. The first Chinese data published seem to show that the symptoms in pregnant women are the same as those of the general population. There are no cases of intrauterine maternal-fetal transmission, but cases of newborns infected early suggest that there could be vertical perpartum or neonatal transmission. Induced prematurity and cases of respiratory distress in newborns of infected mothers have been described. Pregnancy is known as a period at higher risk for the consequences of respiratory infections, as for influenza, so it seems important to screen for Covid-19 in the presence of symptoms and to monitor closely pregnant women. In this context of the SARS-Covid-2 epidemic, the societies of gynecology-obstetrics, infectious diseases and neonatalogy have proposed a French protocol for the management of possible and proven cases of SARS-Covid-2 in pregnant women. These proposals may evolve on a daily basis with the advancement of the epidemic and knowledge in pregnant women. Subsequently, an in-depth analysis of cases in pregnant women will be necessary in order to improve knowledge on the subject. Rosacea is a common, chronic inflammation of sebaceous gland-rich facial skin characterized by severe skin dryness, elevated pH, transepidermal water loss, and decreased hydration levels. Until now, there has been no thorough molecular analysis of permeability barrier alterations in the skin of rosacea patients. Thus, we aimed to investigate the barrier alterations in papulopustular rosacea (PPR) samples compared to healthy sebaceous gland-rich (SGR) skin, using RNASeq analysis (n=8). Pathway analyses by Cytoscape ClueGo revealed 15 significantly enriched pathways related to skin barrier formation. RT-PCR and immunohistochemistry were used to validate the pathway analyses. The results showed significant alterations in barrier components in PPR samples compared to SGR, including the cornified envelope and intercellular lipid lamellae formation, desmosome and tight junction organizations, barrier alarmins, and antimicrobial peptides. Moreover, the barrier damage in PPR was unexpectedly similar to atopic dermatitis (AD); this similarity was confirmed by immunofluorescent staining. In summary, besides the well-known dysregulation of immunological, vascular, and neurological functions, we demonstrated prominent permeability barrier alterations in PPR at the molecular level, which highlight the importance of barrier repair therapies for rosacea. The endogenous increased production of glucocorticoids (GCs) in the skin of the elderly population contributes to age-related defects strikingly similar to those occurring after pharmacological treatments with GCs. GCs act through the ligand-dependent transcription factors GC receptor (GR) and mineralocorticoid receptor (MR). We demonstrated that epidermal MR plays non-redundant roles relative to GR in adult mouse skin homeostasis; however, its relative contribution to natural skin aging has not been previously investigated. 13-month old MR epidermal KO (MREKO) mice showed differential features of aging relative to controls (CO) in all skin compartments. MREKO mice were resistant to age-induced epidermal atrophy but showed reduced dermal thickness, with decreased collagen deposition, and decreased SMAD2/3 activity. Importantly, the dermal white adipose tissue (dWAT) was 2.5-fold enlarged in 13-month MREKOvs CO, featuring adipocyte hyperplasia and hypertrophy, at least in part through early increases in Pparg.