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Pierre Janet's works on conversion disorders or dissociative disorders has mainly fallen to the wayside in favour of Freud's works. In the first part of this paper, Janet's conception of hysteria is discussed and his place in French psychiatry described. Different aspects of Janet's diathesis-stress approach are presented (particularly the pathogenic concept of fixed ideas), which refer not only to a conception of hysteria but also to traumatic (stress) disorders and other psychological disturbances. The second part of the paper details the varieties of Janetian therapeutic treatments of these disorders: the \"liquidation\" of fixed ideas by hypnosis and suggestion, confrontation techniques, which resemble contemporary cognitive behavioural approaches, and special cognitive (\"logagogic\") interventions. Finally, we discuss the various treatment strategies based on psychoeconomic considerations such as physical or psycho-phyical therapies, psychoeducation, treatment through rest, and simplification of life for dealing with basic disturbances of psychic disorders.

This article deals with Pierre Janet's concept of \"Psychological Analysis\" (analyse psychologique). It brings out Janet's criticism of Sigmund Freud's ideas, and delineates the difference between psychological analysis (Janet) and psychoanalysis (Freud). Further it points out that Janet's theories on the pathogenesis of neurotic disorders rely on the concept of psychic trauma and associated fixed ideas. Mental force and mental tension, described in greater detail, are essential for the pathogenesis of mental disorders. According to Janet, a significant characteristic of the neurotically disturbed person is a feature that Von Gebsattel calls \"Werdenshemmung\" (\"inhibition of becoming\"), a state which impairs the life development of the ill person.

Pierre Janet's works on conversion disorders or dissociative disorders has mainly fallen to the wayside in favour of Freud's works. In the first part of this paper, Janet's conception of hysteria is discussed and his place in French psychiatry described. Different aspects of Janet's diathesis-stress approach are presented (particularly the pathogenic concept of fixed ideas), which refer not only to a conception of hysteria but also to traumatic (stress) disorders and other psychological disturbances. The second part of the paper details the varieties of Janetian therapeutic treatments of these disorders: the \"liquidation\" of fixed ideas by hypnosis and suggestion, confrontation techniques, which resemble contemporary cognitive behavioural approaches, and special cognitive (\"logagogic\") interventions. Finally, we discuss the various treatment strategies based on psychoeconomic considerations such as physical or psycho-phyical therapies, psychoeducation, treatment through rest, and simplification of life for dealing with basic disturbances of psychic disorders.

Janet’s conceptions of the subconscious are restrictively conceived but show important differentiations which are discussed in detail. First, an outline of Janet’s conception of consciousness is presented as well as of the terms of psychic synthesis and the notion of the field of consciousness. This is defined as a system of elementary or relatively elementary psychic phenomena which are connected with the personal ego in a given moment. Herbart’s conception of the relation of conscious and unconscious psychic phenomena is analysed. Concerning Janet’s psychology of tendencies, several kinds of subconsciousness are distinguished: dissociative subconsciousness, habit formation, adaptation, psychological automatism, dispositional subconsciousness and threshold-related subconsciousness or subliminal consciousness. The problem of dissociative subconsciousness caused by fixed ideas is discussed, and adaptation, habitualization and psychic automatism are described, all notions which are important for the conception of dissociative subconsciousness. Janet’s understanding of double personality is outlined. Finally, the problem of the threshold of consciousness is explained.

This chapter presents several ways in which Bleuler's concept of schizophrenia is connected to the concept of dissociation. Bleuler criticized Kraepelin's Dementia Preacox, noting that not all cases began early ('praecox') or ended in full mental deterioration. The original concept of schizophrenia, as proposed by Bleuler in 1908 and 1911, was thoroughly infused with concepts of dissociation and the ideas of Pierre Janet. Kurt Schneider proposed a set of symptoms, which he called 'first rank' but have come to be termed 'Schneiderian' as well, to be highly predictive of schizophrenia. In 1970, C. S. Mellor published an influential paper in the British Journal of Psychiatry on the first‐rank symptoms, with detailed descriptions and definitions. Schneider very likely overlooked the presence of dissociative disorders in his schizophrenia group, and attributed dissociative symptoms to a 'breakdown' in the self/world boundary.

This article describes Janet's concept of psychological trauma and the formation of rigid thought complexes (fixed ideas). This concept forms the basis for Janet's functional nosology of the neuroses, and is related to his dynamic psychology of conduct or action. It can be viewed as an early self-regulation model, because it contains a stratified bio-, socio-, and psycho-genetic hierarchy of behavioral \"tendencies\" that produce a more or less adaptive act by means of two hypothesized intervening variables: psychological force and psychological tension. Fixed ideas are viewed within this framework as an outcome of deficient processes of adaptation to psychological trauma. The article closes by pointing out affinities between Janet's psychological concept and modern cognitive and behavioral therapies.

This chapter contains sections titled: Historical overview Important Janetian concepts Schizophrenia Paranoia Hallucinations Assessment and implications References

Superinfections, including invasive pulmonary aspergillosis (IPA), are well-known complications of critically ill patients with severe viral pneumonia. Aim of this study was to evaluate the incidence, risk factors and outcome of IPA in critically ill patients with severe COVID-19 pneumonia. We prospectively screened 32 critically ill patients with severe COVID-19 pneumonia for a time period of 28 days using a standardized study protocol for oberservation of developement of COVID-19 associated invasive pulmonary aspergillosis (CAPA). We collected laboratory, microbiological, virological and clinical parameters at defined timepoints in combination with galactomannan-antigen-detection from nondirected bronchial lavage (NBL). We used logistic regression analyses to assess if COVID-19 was independently associated with IPA and compared it with matched controls. CAPA was diagnosed at a median of 4 days after ICU admission in 11/32 (34%) of critically ill patients with severe COVID-19 pneumonia as compared to 8% in the control cohort. In the COVID-19 cohort, mean age, APACHE II score and ICU mortality were higher in patients with CAPA than in patients without CAPA (36% versus 9.5%; p<0.001). ICU stay (21 versus 17 days; p = 0.340) and days of mechanical ventilation (20 versus 15 days; p = 0.570) were not different between both groups. In regression analysis COVID-19 and APACHE II score were independently associated with IPA. CAPA is highly prevalent and associated with a high mortality rate. COVID-19 is independently associated with invasive pulmonary aspergillosis. A standardized screening and diagnostic approach as presented in our study can help to identify affected patients at an early stage.

Autophagy perturbation represents an emerging therapeutic strategy in cancer. Although LATS1 and LATS2 kinases, core components of the mammalian Hippo pathway, have been shown to exert tumor suppressive activities, here we report a pro-survival role of LATS1 but not LATS2 in hepatocellular carcinoma (HCC) cells. Specifically, LATS1 restricts lethal autophagy in HCC cells induced by sorafenib, the standard of care for advanced HCC patients. Notably, autophagy regulation by LATS1 is independent of its kinase activity. Instead, LATS1 stabilizes the autophagy core-machinery component Beclin-1 by promoting K27-linked ubiquitination at lysine residues K32 and K263 on Beclin-1. Consequently, ubiquitination of Beclin-1 negatively regulates autophagy by promoting inactive dimer formation of Beclin-1. Our study highlights a functional diversity between LATS1 and LATS2, and uncovers a scaffolding role of LATS1 in mediating a cross-talk between the Hippo signaling pathway and autophagy. The autophagic and Hippo pathways are both well characterized contributors to cancer. Here, Tang et al show that LATS1, but not LATS2, negatively regulates autophagy by promoting Beclin1 ubiquitination, which restricts lethal autophagy induced by sorafenib treatment in cancer cells.

Understanding the mechanisms underlying evasive resistance in cancer is an unmet medical need to improve the efficacy of current therapies. In hepatocellular carcinoma (HCC), aberrant expression of hypoxia-inducible factor 1 α (HIF1α) and increased aerobic glycolysis metabolism are drivers of resistance to therapy with the multi-kinase inhibitor Sorafenib. However, it has remained unknown how HIF1α is activated and how its activity and the subsequent induction of aerobic glycolysis promote Sorafenib resistance in HCC. Here, we report the ubiquitin-specific peptidase USP29 as a new regulator of HIF1α and of aerobic glycolysis during the development of Sorafenib resistance in HCC. In particular, we identified USP29 as a critical deubiquitylase (DUB) of HIF1α, which directly deubiquitylates and stabilizes HIF1α and, thus, promotes its transcriptional activity. Among the transcriptional targets of HIF1α is the gene encoding hexokinase 2 (HK2), a key enzyme of the glycolytic pathway. The absence of USP29, and thus of HIF1α transcriptional activity, reduces the levels of aerobic glycolysis and restores sensitivity to Sorafenib in Sorafenib-resistant HCC cells in vitro and in xenograft transplantation mouse models in vivo. Notably, the absence of USP29 and high HK2 expression levels correlate with the response of HCC patients to Sorafenib therapy. Together, the data demonstrate that, as a DUB of HIF1α, USP29 promotes Sorafenib resistance in HCC cells, in parts by upregulating glycolysis, thereby opening new avenues for therapeutically targeting Sorafenib-resistant HCC in patients.