Kroniek van het ondernemingsrecht:Over ondernemingsrecht en 'corporate governance'

In 2016 was er de nodige aandacht voor de maatschappelijke aspecten van ondernemingen en het ondernemingsrecht. Dat is met name tot uitdrukking gekomen in de fundamentele herziening van de Nederlandse Corporate Governance Code, maar ook in de Nota Ondernemingsrecht, die respectievelijk op 8 en 9 december 2016 in finale vorm zijn gepresenteerd. Het onderscheid tussen beursgenoteerde en niet-beursgenoteerde ondernemingen wordt door de Corporate Governance Code gerelativeerd. Dat geldt tevens voor grote non-profit organisaties, die ook overigens steeds meer gelijk worden behandeld met naamloze en besloten vennootschappen bijvoorbeeld als het gaat om aansprakelijkheid van bestuurders en commissarissen of leden van een raad van toezicht. Specifiek met het oog daarop is in 2016 het wetsvoorstel Bestuur en toezicht rechtspersonen ingediend. Wat betreft rechtspraak wordt naast corporate governance, aandacht besteed aan de lage drempels voor ontvankelijkheid bij de Ondernemingskamer, aansprakelijkheid van bestuurders van rechtspersonen en vereenzelviging van rechtspersonen, doorwerking van aandeelhoudersovereenkomsten in vennootschapsrechtelijke toetsing en toetsing van dividendbesluiten. Aan de hand van jurisprudentie van de Ondernemingskamer wordt tevens het creatieve gebruik van de bevoegdheden door de Ondernemingskamer geïllustreerd

Metabolomics signatures of depression:the role of symptom profiles

Depression shows a metabolomic signature overlapping with that of cardiometabolic conditions. Whether this signature is linked to specific depression profiles remains undetermined. Previous research suggested that metabolic alterations cluster more consistently with depressive symptoms of the atypical spectrum related to energy alterations, such as hyperphagia, weight gain, hypersomnia, fatigue and leaden paralysis. We characterized the metabolomic signature of an "atypical/energy-related" symptom (AES) profile and evaluated its specificity and consistency. Fifty-one metabolites measured using the Nightingale platform in 2876 participants from the Netherlands Study of Depression and Anxiety were analyzed. An 'AES profile' score was based on five items of the Inventory of Depressive Symptomatology (IDS) questionnaire. The AES profile was significantly associated with 31 metabolites including higher glycoprotein acetyls (β = 0.13, p = 1.35*10 -12), isoleucine (β = 0.13, p = 1.45*10 -10), very-low-density lipoproteins cholesterol (β = 0.11, p = 6.19*10 -9) and saturated fatty acid levels (β = 0.09, p = 3.68*10 -10), and lower high-density lipoproteins cholesterol (β = -0.07, p = 1.14*10 -4). The metabolites were not significantly associated with a summary score of all other IDS items not included in the AES profile. Twenty-five AES-metabolites associations were internally replicated using data from the same subjects (N = 2015) collected at 6-year follow-up. We identified a specific metabolomic signature-commonly linked to cardiometabolic disorders-associated with a depression profile characterized by atypical, energy-related symptoms. The specific clustering of a metabolomic signature with a clinical profile identifies a more homogenous subgroup of depressed patients at higher cardiometabolic risk, and may represent a valuable target for interventions aiming at reducing depression's detrimental impact on health. </p

Metabolomic profiles discriminating anxiety from depression

Objective: Depression has been associated with metabolomic alterations. Depressive and anxiety disorders are often comorbid diagnoses and are suggested to share etiology. We investigated whether differential metabolomic alterations are present between anxiety and depressive disorders and which clinical characteristics of these disorders are related to metabolomic alterations. Methods: Data were from the Netherlands Study of Depression and Anxiety (NESDA), including individuals with current comorbid anxiety and depressive disorders (N = 531), only a current depression (N = 304), only a current anxiety disorder (N = 548), remitted depressive and/or anxiety disorders (N = 897), and healthy controls (N = 634). Forty metabolites from a proton nuclear magnetic resonance lipid-based metabolomics panel were analyzed. First, we examined differences in metabolites between disorder groups and healthy controls. Next, we assessed whether depression or anxiety clinical characteristics (severity and symptom duration) were associated with metabolites. Results: As compared to healthy controls, seven metabolomic alterations were found in the group with only depression, reflecting an inflammatory (glycoprotein acetyls; Cohen's d = 0.12, p = 0.002) and atherogenic-lipoprotein-related (e.g., apolipoprotein B: Cohen's d = 0.08, p = 0.03, and VLDL cholesterol: Cohen's d = 0.08, p = 0.04) profile. The comorbid group showed an attenuated but similar pattern of deviations. No metabolomic alterations were found in the group with only anxiety disorders. The majority of metabolites associated with depression diagnosis were also associated with depression severity; no associations were found with anxiety severity or disease duration. Conclusion: While substantial clinical overlap exists between depressive and anxiety disorders, this study suggests that altered inflammatory and atherogenic-lipoprotein-related metabolomic profiles are uniquely associated with depression rather than anxiety disorders

Marked TGF-β-regulated miRNA expression changes in both COPD and control lung fibroblasts

© 2019, The Author(s). COPD is associated with disturbed tissue repair, possibly due to TGF-β-regulated miRNA changes in fibroblasts. Our aim was to identify TGF-β-regulated miRNAs and their differential regulation and expression in COPD compared to control fibroblasts. Small RNA sequencing was performed on TGF-β-stimulated and unstimulated lung fibroblasts from 15 COPD patients and 15 controls. Linear regression was used to identify TGF-β-regulated and COPD-associated miRNAs. Interaction analysis was performed to compare miRNAs that responded differently to TGF-β in COPD and control. Re-analysis of previously generated Ago2-IP data and Enrichr were used to identify presence and function of potential target genes in the miRNA-targetome of lung fibroblasts. In total, 46 TGF-β-regulated miRNAs were identified in COPD and 86 in control fibroblasts (FDR < 0.05). MiR-27a-5p was the most significantly upregulated miRNA. MiR-148b-3p, miR-589-5p and miR-376b-3p responded differently to TGF-β in COPD compared to control (FDR < 0.25). MiR-660-5p was significantly upregulated in COPD compared to control (FDR < 0.05). Several predicted targets of miR-27a-5p, miR-148b-3p and miR-660-5p were present in the miRNA-targetome, and were mainly involved in the regulation of gene transcription. In conclusion, altered TGF-β-induced miRNA regulation and differential expression of miR-660-5p in COPD fibroblasts, may represent one of the mechanisms underlying aberrant tissue repair and remodelling in COPD