Components of the biochemical inflammatory response (COX-2, PGE<sub>2</sub>, TBARS, 15d-PGJ<sub>2</sub>, ERK, p65 NFκB) and glucocorticoid receptor -GR- expression and the scores on the impulsivity measures in the BARRATT, EDI and BITE questionnaires showed a significant correlation within the AN patients group.
Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group.
Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group.
Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group.
Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group.
These changes, supported by altered mRNA levels of genes coding for enzymes involved in eiCs-related methabolic pathways (i.e., PLA<sub>2</sub>, COX-2, 5-LOX and 15-LOX), underlie a widespread brain dysregulation of pro- and anti-inflammatory eiC-mediated processes in the ABA model of AN.
Plasma levels of the pro-inflammatory cytokines TNF-α and IL-1β were significantly increased in patients with AN, while the levels of prostaglandins PGE<sub>2</sub> (proinflammatory) and 15d-PGJ<sub>2</sub>, (anti-inflammatory) were lower compared with controls.
Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group.
Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group.
Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group.
These changes, supported by altered mRNA levels of genes coding for enzymes involved in eiCs-related methabolic pathways (i.e., PLA<sub>2</sub>, COX-2, 5-LOX and 15-LOX), underlie a widespread brain dysregulation of pro- and anti-inflammatory eiC-mediated processes in the ABA model of AN.
Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group.
Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group.
Ninety-four female adolescent inpatients with restricting anorexia nervosa (AN-R), 67 with binge/purge AN (AN-B/P), and 48 with bulimia nervosa (BN) were assessed on admission and discharge using the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), Yale-Brown-Cornell Eating Disorders Scale (YBC-EDS), Eating Attitude Test-26 (EAT-26), Beck Depression Inventory (BDI), and State-Trait Anxiety Inventory (STAI).
Here, we used a battery of methods (LD score regression, genetic risk scores, sign test, SNP effect concordance analysis, and Mendelian randomization) to investigate the genetic covariation between subcortical brain volumes and risk for AN based on summary measures retrieved from genome-wide association studies of regional brain volumes (ENIGMA consortium, n = 13,170) and genetic risk for AN (PGC-ED consortium, n = 14,477).
Following on from previous work by our group where we showed that early onset anorexia nervosa (AN) and obsessive-compulsive disorder (OCD) shared a common genetic background, the aim of the present study is to assess genetic pleiotropy related to the serotonergic system (SLC6A4, 5HTR2A, 5HTR2C, TPH2, SLC18A1), in a common phenotype such as very-early age of onset.
This study investigated a possible correlation between opiorphin and stress/immune biomarkers, cortisol, salivary alpha-amylase (sAA) and secretory immunoglobulin A (sIgA), in saliva of patients with restrictive-type AN.
A decrease of body mass index (BMI)-SDS increased the risk for comorbid anorexia nervosa (7.1-fold [95% CI 3.6-14.3] compared with stable BMI-SDS, 6.9-fold [95%CI 3.4-14.1] compared with increase of BMI-SDS).
A secondary osteoporosis associated with the VFC was diagnosed in 52 patients: glucocorticoid-induced osteoporosis (25.7%), non-malignant hemopathies (6.2%), alcoholism (4.4%), use of aromatase inhibitors (3.6%), primary hyperparathyroidism (2.7%), hypercorticism (2.7%), anorexia nervosa (2.7%), and pregnancy and lactation-associated osteoporosis (1.8%).
Changes in Microbiota and Bacterial Protein Caseinolytic Peptidase B During Food Restriction in Mice: Relevance for the Onset and Perpetuation of Anorexia Nervosa.