Question For decades hysteria has been psychodynamically interpreted sexualized as part of a frustrated desire with a depressive core. However, this "victim" side should be faced with the other often hidden aspects of hysteria with aggression and striving for power. Method The basic hypothesis pursued here is that the hysterical/histrionic person was not primarily "disadvantaged" in his or her development, but that his or her striving for power and thus his or her potential for aggression is to be understood above all as a learned mode of global relationship that the adolescents have learned to respond and assert themselves to an intra-familiar situation of tension and pressure. Results Any therapy that does not take this sufficiently into account falls short and reinforces the underlying mechanism of the therapeutic relationship dynamics. During treatment the patient must increasingly feel how much destruction and loneliness this global relationship implies. Conclusions Only if the patient experiences that reduction of dominance and self-reference as well as increase of "true" felt empathy lead to more satisfying relations, the "imprisonment" in hysterical mode can be gradually lifted.Objectives This study aimed to investigate the effect of waiting for inpatient psychosomatic psychotherapy and the prediction of treatment outcome from the effect of waiting in depressed patients. Methods A total of N = 519 patients were assessed for depressive symptoms before their initial intake interview, at the time of their hospital admission (on average 6 weeks after the intake), and at discharge (after eight weeks of inpatient psychotherapy). Results There was a small to moderate reduction in depressive symptoms from intake interview to hospital admission. This effect was independent from the waiting duration. Latent change from intake interview to hospital admission was a significant moderate predictor of treatment outcome at discharge. Conclusions Findings imply that the prospect of inpatient psychotherapy may affect patients' depression severity. Furthermore, patients who benefit more from the prospect of treatment may also achieve higher therapeutic effects.Background and purpose - Femoroacetabular impingement syndrome (FAIS) is a common cause of hip pain and may contribute to the development of osteoarthritis. We investigated whether a prior hip arthroscopy affects the patient-reported outcomes (PROMs) of a later total hip arthroplasty (THA).Patients and methods - Patients undergoing hip arthroscopy between 2011 and 2018 were identified from a hip arthroscopy register and linked to the Swedish Hip Arthroplasty Register (SHAR). A propensity-score matched control group without a prior hip arthroscopy, based on demographic data and preoperative score from the EuroQoL visual analogue scale (EQ VAS) and hip pain score, was identified from SHAR. The group with a hip arthroscopy (treated group) consisted of 135 patients and the matched control group comprised 540 patients. The included PROMs were EQ-5D and EQ VAS of the EuroQoL group, and a questionnaire regarding hip pain and another addressing satisfaction. Rate of reoperation was collected from the SHAR. The follow-up period was 1 year.Results - The mean interval from arthroscopy to THA was 27 months (SD 19). The EQ-5D was 0.81 and 0.82, and EQ VAS was 78 and 79 in the treated group and the matched control group respectively. GO-203 molecular weight There were no differences in hip pain, and reported satisfaction was similar with 87% in the treated group and 86% in the matched control group.Interpretation - These results offer reassurance that a prior hip arthroscopy for FAIS does not appear to affect the short-term patient-reported outcomes of a future THA and indicate that patients undergoing an intervention are not at risk of inferior results due to their prior hip arthroscopy.Sphingosine kinase 1 (SphK1) and sphingosine-1-phosphate (S1P) signaling regulates numerous diseases such as cancer, diabetes, and inflammation-related ailments, rheumatoid arthritis, atherosclerosis, and multiple sclerosis. The importance of SphK1 in chemo-resistance has been extensively explored in breast, lung, colon, and hepatocellular carcinomas. SphK1 is considered an attractive drug target for the development of anticancer therapy. New drug molecules targeting the S1P signaling are required owing to its pleiotropic nature and association with multiple downstream targets. Here, we have investigated the binding affinity and SphK1 inhibitory potential of cinchonine and colcemid using a combined molecular docking and simulation studies followed by experimental analysis. These compounds bind to SphK1 with a significantly high affinity and subsequently inhibit kinase activity (IC50 7-9 μM). Further, MD simulation studies revealed that both cinchonine and colcemid bind to the residues at the active site pocket of SphK1 with several non-covalent interactions, which may be responsible for inhibiting its kinase activity. Besides, the binding of cinchonine and colcemid causes substantial conformational changes in the structure of SphK1. Taken together, cinchonine and colcemid may be implicated in designing potential drug molecules with improved affinity and specificity for SphK1 targeting anticancer therapy.Communicated by Ramaswamy H. Sarma.Approximately 14% of the general population suffer from chronic kidney disease that can lead to acute kidney injury (AKI), a condition with up to 50% mortality for which there is no effective treatment. Hypertension, diabetes, and cardiovascular disease are the main comorbidities, and more than 660,000 Americans have kidney failure. β2-Adrenergic receptors (β2ARs) have been extensively studied in association with lung and cardiovascular disease, but with limited scope in kidney and renal diseases. β2ARs are expressed in multiple parts of the kidney including proximal and distal convoluted tubules, glomeruli, and podocytes. Classical and noncanonical β2AR signaling pathways interface with other intracellular mechanisms in the kidney to regulate important cellular functions including renal blood flow, electrolyte balance and salt handling, and tubular function that in turn exert control over critical physiology and pathology such as blood pressure and inflammatory responses. Nephroprotection through activation of β2ARs has surfaced as a promising field of investigation; however, there is limited data on the pharmacology and potential side effects of renal β2AR modulation.