treatment targeting IL-17 pathway. Immunocytofluorimetric markers may contribute to a personalized therapy in COVID patients.

Intensive care unit-acquired weakness (ICU-AW) is a complex spectrum of disability that delays recovery of critically ill-immobilized patients with sepsis. Much discrepancy remain on the use of corticosteroids and their impact on muscle regeneration in critical illness management. Therefore, the aim of this study is to investigate whether hydrocortisone (HCT) modulates muscle mass turnover in ICU-AW induced by sepsis with limb immobilization (SI).

Sepsis by cecal ligation puncture (CLP) with forelimb-immobilization were performed in rats. The study consisted of four groups Sham (left forelimb-immobilization), Sham HCT (left forelimb-immobilization + HCT), SI (CLP+left forelimb-immobilization) and SI HCT (CLP+left forelimb-immobilization + HCT). Motor force, blood and muscle sampling were assessed.

HCT prevented body weight loss associated with SI and attenuated systemic and muscular inflammation. Besides, myosin was restituted in SI HCT group in conjunction to muscle mass and strength restoration. Pro-hypertrophic calcineurin (PP2B-Aβ) and nuclear factor of activated T-cells C3 (NFATc3) but not protein kinase B (Akt) were re-activated by HCT. Finally, pro-atrophic extracellular signal-regulated kinases (ERK1/2) and p38 mitogen-activated protein kinases (p38) but not nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) were inhibited in SI HCT group.

This study unravels new molecular events thought to control muscle protein synthesis in ICU-AW induced by sepsis and limb immobilization. HCT has a potential to fine-tune muscle-signaling pathways and to reduce the negative outcomes of ICU-AW.

This study unravels new molecular events thought to control muscle protein synthesis in ICU-AW induced by sepsis and limb immobilization. HCT has a potential to fine-tune muscle-signaling pathways and to reduce the negative outcomes of ICU-AW.Ischemic stroke represents a serious medical condition which could cause survivors suffer from long-term and even lifetime disabilities. After a stroke attack, the brain would undergo varying degrees of recovery, in which the central nervous system could be reorganized spontaneously or with the help of appropriate rehabilitation. Magnetic resonance imaging (MRI) is a non-invasive technique which can provide comprehensive information on structural, functional and metabolic features of brain tissue. In the last decade, there has been an increased technical advancement in MR techniques such as voxel-based morphological analysis (VBM), diffusion magnetic resonance imaging (dMRI), functional magnetic resonance imaging (fMRI), arterial spin-labeled perfusion imaging (ASL), magnetic sensitivity weighted imaging (SWI), quantitative sensitivity magnetization (QSM) and magnetic resonance spectroscopy (MRS) which have been proven to be a valuable tool to study the brain tissue reorganization. Due to MRI indices of neuroplasticity related to neurological outcome could be translated to the clinic. The ultimate goal of this review is to equip readers with a fundamental understanding of advanced MR techniques and their corresponding clinical application for improving the ability to predict neuroplasticity that are most suitable for stroke management.There is considerable concern that naphthenic acids (NA) related to oil extraction can negatively impact reproduction in mammals, yet the mechanisms are unknown. ONC201 Since placental dysfunction is central to many adverse pregnancy outcomes, the goal of this study was to determine the effects of NA exposure on placental trophoblast cell function. HTR-8/SVneo cells were exposed to a commercial technical NA mixture for 24 hours to assess transcriptional regulation of placentation-related pathways and functional assessment of migration, invasion, and angiogenesis. Pathway analysis suggests that NA treatment resulted in increased epithelial-to-mesenchymal transition. However, there was reduced migration and invasive potential. NA treatment increased angiogenesis-related pathways with a concomitant increase in tube formation. Since decreased trophoblast invasion/migration and aberrant angiogenesis have been associated with placental dysfunction, these findings suggest that it is biologically plausible that exposure to NA may result in altered placental development and/or function.GLP-1 receptor agonists are used for the treatment of type 2 diabetes but they may reduce appetite and cause nausea and emesis. We investigated if GLP-1 (7-36) amide can modulate glucose homoeostasis, emesis and feeding via an exendin (9-39)-sensitive mechanism in Suncus murinus. The effect of GLP-1 (7-36) amide on glucose homeostasis was examined using an intraperitoneal glucose tolerance test. In conscious fasted animals, food and water consumption and behavior were measured for 1 h following drug administration. c-Fos expression in the brain was measured using immunohistochemistry. GLP-1 (7-36) amide reduced blood glucose levels dose-dependently. Exendin (9-39) did not modify blood glucose levels but suppressed the glucose-lowering effect of GLP-1 (7-36) amide. GLP-1 (7-36) amide inhibited food and water intake, induced emesis and elevated c-Fos expression in the brainstem and hypothalamic nuclei in the brain. Exendin (9-39) antagonised the inhibition of food and water intake and emesis induced by GLP-1 (7-36) amide and the effects on c-Fos expression in the hypothalamus and brainstem, excepting for the bed nucleus of the stria terminalis. These data suggest that the action of GLP-1 (7-36) amide to modulate blood glucose, suppress food and water intake and induce emesis involve GLP-1 receptors in the hypothalamus and brainstem.This study aimed at investigating whether treatment with icariin (ICA) could modulate the progression of experimental autoimmune encephalomyelitis (EAE) and its potential mechanisms in SJL/J mice. Female SJL/J mice were immunized with PLP139-151 peptide to induce relapse-remitting EAE and the immunized mice were treated with vehicle alone (EAE) or ICA (12.5 or 25 mg/body weights) by gavage daily for 42 days. Compared with the control, the EAE mice developed relapse-remitting EAE and reduced body weights (15.76 ± 0.61 vs. 17.60 ± 0.98 g on day 13; 17.35 ± 0.44 vs. 18.46 ± 0.66 g on day 26), accompanied by severe inflammation with many microglia infiltrates and obvious demyelination in the spinal cord tissues. Conversely, ICA treatment significantly reduced the clinical scores (on day 13, 1.00 ± 0.16 and 1.10 ± 0.33 for ICA 12.5 and 25 mg/kg group, respectively vs. 1.62 ± 0.41 in the EAE group; on day 26, 0.50 ± 0.23 and 0.40 ± 0.24 for ICA 12.5 and 25 mg/kg group, respectively, vs. 1.56 ± 0.29 in the EAE group), mitigated the body weight reduction, spinal cord inflammation and demyelination in EAE mice (pathological scores of 2.