Establishing the substantive interpretation of the GFP by considering evidence from research on personality disorders and Animal Personality

In research on individual differences, various structural models aim at providing a comprehensive description of personality. These models assume multiple, mostly independent personality dimensions. More recently, the so-called General Factor of Personality (GFP) has become a proliferous, but contentious, topic. The notion of the GFP is based on the observations that personality dimensions are not independent, but in fact show consistent inter-correlations, leading to a relevant proportion of shared variance among them (Figueredo et al., 2006). The GFP seems to capture the socially desirable ends of personality scales, and, in terms of the Big Five model, high-GFP individuals score relatively high on openness, conscientiousness, extraversion (mainly the sociability-facet), agreeableness, and emotional stability (Rushton and Irwing, 2009; van der Linden et al., 2010a). Some authors have suggested that the GFP simply reflects methodological artifacts (Ashton et al., 2009; Backstrom et al., 2009; Hopwood et al., 2011b; Pettersson et al., 2012). However, much of this criticism has been addressed (Rushton and Erdle, 2010; Loehlin, 2012; Dunkel and van der Linden, 2014; van der Linden et al., 2014a). The objective of the present work is not to reiterate these issues, as they have been discussed extensively elsewhere (Irwing, 2013; van der Linden et al., 2016). Instead, we contend that criticism mostly offered within the specialty of personality psychology misses the bigger picture. More specific, evidence in favor of the GFP as a substantive and theoretically coherent construct has been provided in other research fields long before it became a contentious issue in personality psychology. Here we introduce two lines of evidence that may further corroborate the substantive interpretation of the GFP, specifically, findings from personality pathology as well as from animal personality. Looking at the GFP from a different perspective may help to overcome the current debates within personality psychology. In the following we will first briefly introduce work on the GFP and its theoretical foundation as social effectiveness. Afterwards we outline research from psychiatric nosology and animal ecology and discuss these in context

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases. Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies. It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios. Thus far, dozens of methods have been proposed to quantify cell death-related parameters. However, no guidelines exist regarding their use and interpretation, and nobody has thoroughly annotated the experimental settings for which each of these techniques is most appropriate. Here, we provide a nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls. These guidelines are intended for investigators who study cell death, as well as for reviewers who need to constructively critique scientific reports that deal with cellular demise. Given the difficulties in determining the exact number of cells that have passed the point-of-no-return of the signaling cascades leading to cell death, we emphasize the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells

Supplementary Material for: Antidepressant Use Prospectively Relates to a Poorer Long-Term Outcome of Depression: Results from a Prospective Community Cohort Study over 30 Years

Medicin

Big Five Personality Traits and the General Factor of Personality as Moderators of Stress and Coping Reactions Following an Emergency Alarm on a Swiss University Campus

We conducted an online survey including 306 participants aged 18-64years to assess the general factor of personality (GFP) and Big Five personality traits in relation to individual stress and coping reactions following a shooting emergency alarm at a Swiss university campus. Although the emergency eventually turned out to be a false alarm, various witnesses showed pronounced distress owing to a vast police operation. The GFP structure was replicated using two alternative modelling approaches. Neuroticism related substantially to acute fear and traumatic distress as well as to more enduring maladaptive coping. Agreeableness was negatively associated with the coping strategy of medication use, whereas both agreeableness and conscientiousness related positively to social activity following the emergency. The GFP related moderately to peri-traumatic distress and showed a substantial negative association with medication use and a strong positive association with social activity. In conclusion, both the GFP and Big Five traits significantly moderate stress responses following a stressful life event. The GFP predominantly relates to socially adaptive coping, whereas in particular neuroticism accounts for acute stress reactions such as fear and traumatic distress. These findings support the notion that personality influences how persons react in the face of adversity

Zusammenhang zwischen Burnout und Persönlichkeit

BACKGROUND: The causes of burnout can be mainly ascribed to stressful working conditions. Research results concerning the influence of personality characteristics on the risk of burnout are rare. Research addressing the interaction of the person and the environment on the risk of burnout is needed. METHODS: This study analysed data from the Zürich study. This study of a cohort from the general population started in 1978, when the participants were 19 and 20 years old and followed them until the age of 49 and 50. In the last interview (2008) several dimensions of burnout were assessed for the first time. The association between burnout and coping (mastery and self-confidence) on the one hand and personality characteristics as assessed in 1988 by means of the Freiburg Personality Inventory on the other were analysed. RESULTS: In a path-analytical model various associations between the variables under investigation were found. The results identify a complex interaction between a dysfunctional, maladaptive personality and burnout. CONCLUSIONS: More samples from the general population are needed to better understand the interaction between person and environment on the risk of burnout

Apoptotic cell death in disease-Current understanding of the NCCD 2023

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease

Farnesyl Transferase Inhibitors Enhance Death Receptor Signals and Induce Apoptosis in Multiple Myeloma Cells

Multiple myeloma is an incurable plasma cell malignancy in which Ras may be constitutively active either via interleukin-6 (IL-6) receptor signaling or by mutation. Inactivation of Ras may be achieved with farnesyl transferase (FTase) inhibitors a class of drugs which have shown promise in clinical trials particularly in patients with acute leukemia. This report investigates the efficacy of two distinct classes of FTase inhibitors in diverse myeloma cell lines and primary isolates. While Ras signaling has traditionally been linked to myeloma cell growth, we found that these compounds also potently triggered cell death. Death induced by perillic acid (PA) was caspase dependent without evidence of death receptor activation. Apoptosis was associated with mitochondrial membrane depolarization and activation of caspase-9 and 3 but proceeded despite over-expression of Bcl-X L a known correlate of relapsed and chemorefractory myeloma. In addition, Fas ligand and TRAIL mediated apoptosis was potentiated in death receptor resistant (U266) and sensitive (RPMI 8226/S) cell lines. Of clinical relevance, the FTase inhibitor R115777 induced cell death in myeloma lines at doses observed in clinical trials. Furthermore, both R115777 and PA induced cell death in primary isolates with relative specificity. Taken together these preclinical data provide evidence that FTase inhibitors may be an effective therapeutic modality for the treatment of multiple myeloma