1,293 publications from this institution
The authors report on the case of a 5,8 year-old girl whose father died of medullary thyroid carcinoma. When she was 4,5 year-old, her physical examination was normal but plasma calcitonin and katacalcin (PDN-21) levels were abnormally high in response to pentagastrin infusion. Total thyroidectomy was performed and immunohistochemical staining showed confluent C-cell hyperplasia. No recurrence occurred in this patient over four years on follow-up.
Abstract. In protein-calorie malnutrition, serum IGF-I concentrations are low despite high GH. This GH resistance might be due to a reduced number of liver GH binding sites as suggested by studies performed in fasted rats that were refed a low protein diet. To determine whether a postreceptor defect in GH action might also contribute to the GH resistance, we measured the number and the affinity constant of the liver GH binding sites and the serum IGF-I responses to injections of recombinant bGH in hypophysectomized female rats, fed a standard (15% protein) diet (N = 25) or a low (5%) protein diet (N = 25) for 8 days. There were no significant differences in the liver GH binding capacities between the 15% and the 5% protein-fed rats, whether expressed as pmol per liver (20.6 ± 3.5 vs 14.4 ± 1.3; mean ± sem ; P < 0.2; N = 5, respectively), pmol per mg DNA (1.08 ± 0.16 vs 0.84 ± 0.07; P <0.4) or fmol per mg of protein (28.98 ± 5.04 vs 30.26 ± 2.00; P > 0.5). Likewise, the affinity constants of the GH binding sites of the 15% and the 5% protein-fed rats were not significantly different (0.78 ± 0.05 vs 0.78 ± 0.07 × 10 9 l/mol; P > 0.5). Despite these non-significant reductions in liver GH binding sites, the IGF-I responses 24 h after sc injections of increasing doses of bovine GH were blunted in the rats fed the 5% protein diet. The maximal IGF-I response in the rats with the normal protein intake was 360 ± 30 U/I, but only 130 ± 40 U/l in the 5% protein-fed animals ( P < 0.001). The blunted serum IGF-I responses to GH, together with decreased maximal stimulation in the 5% protein-fed hypophysectomized rats, support the possibility that a postreceptor defect in GH action contributes to the GH resistance in protein-calorie malnutrition.
Abstract The top-down DSM/ICD categories of mood disorders are inaccurate, and their dogmatic nature precludes both deductive (as indisputable) and inductive (as top-down) remodeling of case definitions. In trials, psychiatric rating scale scores employed as outcome variables are invalid and rely on folk psychology-like narratives. Using machine learning techniques we developed a new precision nomothetic model of mood disorders with a recurrence of illness (ROI) index, a new endophenotype class, namely Major Dysmood Disorder (MDMD), characterized by increased ROI, a more severe phenome, and more disabilities Nonetheless, our previous studies did not compute Research and Diagnostic Algorithmic Rules (RADAR) to diagnose MDMD and score ROI, lifetime (LT), and current suicidal behaviors, as well as the phenome of mood disorders. Here we provide rules to compute bottom-up RADAR scores for MDMD, ROI, lifetime (LT) and current suicidal SI and SA, the phenome of mood disorders, and the lifetime trajectory of mood disorder patients from a family history of mood disorders and substance abuse to adverse childhood experiences, ROI, and the phenome. We also demonstrate how to plot the 12 major scores in a single RADAR graph, which displays all features in a two-dimensional plot. These graphs allow the characteristics of a patient to be displayed as an idiomatic fingerprint, allowing one to estimate the key traits and severity of the illness at a glance. Consequently, biomarker research into mood disorders should use our RADAR scores to examine pan-omics data, which should be used to enlarge our precision models and RADAR graph.
Department of Psychiatry and Neuropsychology, University of Maastricht, Maastricht, The Netherlands, Clinical Research Centre for Mental Health, Antwerp, Belgium, Department of Psychiatry, Vanderbilt University, Nashville, USA and the IRCCS, Fatebenefratelli, Brescia, Italy Correspondence to Michael Maes, MD, PhD, Professor and Chairman, Department of Psychiatry and Neuropsychology, University Hospital of Maastricht, Postbus 5800, 6202 AZ Maastricht, The Netherlands. Tel: +31 43 387 7443; fax: +31 43 387 5444; e-mail: [email protected]
