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Background: Post-stroke emotionalism affects one in five stroke sufferers 6 months after their stroke, but despite its frequency remains a poorly understood stroke symptom. The literature is limited, especially compared to other frequently observed neurological conditions such as aphasia and visual neglect. Aim and Methods: This narrative review presents a summary of the post-stroke emotionalism literature, to inform clinical practice and future research. We cover discussion of definitions, prevalence, neurobiology, predisposing and precipitating factors, and treatment. Results: Increasing evidence suggests that damage to specific areas functionally linked to emotion expression or regulation processes, disruption to structural pathways and those related to serotonin production and modulation individually or in concert give rise to emotionalism-type presentations. A range of emotionalism measurement tools have been used in research contexts making between study comparisons difficult. Testing for Emotionalism after Recent Stroke–Questionnaire (TEARS-Q) has recently been developed to allow standardized assessment. Treatment options are limited, and there have been few adequately powered treatment trials. Antidepressants may reduce severity, but more trial data are required. There have been no randomized-controlled trials of non-pharmacological interventions. Conclusions: More research is needed to improve recognition and treatment of this common and disabling symptom. We conclude with research priorities and recommendations for the field. [ABSTRACT FROM AUTHOR]

An open group intervention for stroke inpatients, based on Acceptance and Commitment Therapy, is evaluated using retrospective clinical service data. Participants were included unless severely unwell or unable to provide informed consent. 117 participants attended at least two sessions in a non-controlled, repeated measures design. Two session protocols were delivered on alternating weeks by an Assistant Psychologist and Trainee Psychologist, covering values, committed action, and acceptance. Participants rated their mood each session using the Depression Intensity Scale Circles (DISCs). Attended sessions ranged from 1 to 11 (Md: 2). Significant reductions in DISCs scores with medium effect sizes were found among those scoring above the cut-off for depression at baseline, Χ2(3) = 20.87, p <.001. The likelihood of scoring below the cut-off for depression did not change between participants' first and last sessions, X2(1, N = 117) = 1.36, p =.24. The number of sessions attended did not predict outcome, rs(117) =.09, p =.33. Design limitations prevented inferences of clinical effectiveness, but the group met several clinical utility criteria by providing a flexible intervention on a rehabilitation ward with competing demands. We highlight the importance of contrasting findings of clinical trials with data from clinical services. In an uncontrolled, within-subjects analysis, we found that attendance of an open-group Acceptance and Commitment Therapy (ACT) based intervention was associated with reduced depressive symptoms in stroke rehabilitation inpatients Open-group psychological interventions may be an accessible and low-cost option for stroke clinicians on inpatient wards where flexibility is important [ABSTRACT FROM AUTHOR]

Obstructive and nonobstructive forms of hydronephrosis (increased diameter of the renal pelvis and calyces) and hydroureter (dilatation of the ureter) are the most frequently detected antenatal abnormalities, yet the underlying molecular mechanisms are largely undefined. Hedgehog (Hh) proteins control tissue patterning and cell differentiation by promoting GLI-dependent transcriptional activation and by inhibiting the processing of GLI3 to a transcriptional repressor. Genetic mutations that generate a truncated GLI3 protein similar in size to the repressor in humans with Pallister-Hall syndrome (PHS; a disorder whose characteristics include renal abnormalities) and hydroureter implicate Hh-dependent signaling in ureter morphogenesis and function. Here, we determined that Hh signaling controls 2 cell populations required for the initiation and transmission of coordinated ureter contractions. Tissue-specific inactivation of the Hh cell surface effector Smoothened (Smo) in the renal pelvic and upper ureteric mesenchyme resulted in nonobstructive hydronephrosis and hydroureter characterized by ureter dyskinesia. Mutant mice had reduced expression of markers of cell populations implicated in the coordination of unidirectional ureter peristalsis (specifically, Kit and hyperpolarization-activation cation-3 channel [Hcn3]), but exhibited normal epithelial and smooth muscle cell differentiation. Kit deficiency in a mouse model of PHS suggested a pathogenic role for GLI3 repressor in Smo-deficient embryos; indeed, genetic inactivation of Gli3 in Smo-deficient mice rescued their hydronephrosis, hydroureter, Kit and Hcn3 expression, and ureter peristalsis. Together, these data demonstrate that Hh signaling controls Kit and Hcn3 expression and ureter peristalsis., Introduction Congenital dilatation of the urinary tract, defined as increased diameter of the renal pelvis (hydronephrosis) with or without dilatation of the ureter (hydroureter), is the most frequently detected abnormality [...]

Aim: This study aims to assess surgical outcomes and survival following first, second and third pelvic exenterations for pelvic malignancy. Method: Consecutive patients undergoing pelvic exenteration for pelvic malignancy at a quaternary referral centre from January 1994 and December 2017 were included. Demographics and surgical outcomes were compared between patients who underwent first, second and third pelvic exenterations by generalized mixed modelling with repeated measures. Survival was assessed using Cox proportional hazards models and Kaplan–Meier plots. Results: Of the 642 exenterations reviewed, 29 (4.5%) were second and 6 (0.9%) were third exenterations. Patients selected for repeat exenteration were more likely to have asymptomatic local recurrences detected on routine surveillance (P < 0.001). Postoperative wound complications increased with repeat exenteration (6%, 17%, 33%; P = 0.003, respectively). Additionally, postoperative length of stay increased from 27 to 38 and 48 days, respectively (P = 0.004). Median survival from first exenteration was 4.75, 5.30 and 8.14 years respectively amongst first, second and third exenteration cohorts (P = 0.849). Median survival from the most recent exenteration was 4.75 years after a first exenteration, 2.02 years after a second exenteration and 1.45 years after a third exenteration (P = 0.0546). Conclusion: This study demonstrates that repeat exenteration for recurrent pelvic malignancy is feasible but is associated with increased complication rates and length of admission and reduced likelihood of attaining R0 margin. Moreover, these data indicate that repeat exenteration does not afford a survival advantage compared with patients having a single exenteration. These data suggest that repeat exenteration for recurrent pelvic malignancy may be of questionable therapeutic value. [ABSTRACT FROM AUTHOR]

Normal kidney function depends on the proper development of the nephron: the functional unit of the kidney. Reciprocal signaling interactions between the stroma and nephron progenitor compartment have been proposed to control nephron development. Here, we show that removal of hedgehog intracellular effector smoothened ( Smo -deficient mutants) in the cortical stroma results in an abnormal renal capsule, and an expanded nephron progenitor domain with an accompanying decrease in nephron number via a block in epithelialization. We show that stromal-hedgehog-Smo signaling acts through a GLI3 repressor. Whole-kidney RNA sequencing and analysis of FACS-isolated stromal cells identified impaired TGFβ2 signaling in Smo -deficient mutants. We show that neutralization and knockdown of TGFβ2 in explants inhibited nephrogenesis. In addition, we demonstrate that concurrent deletion of Tgfbr2 in stromal and nephrogenic cells in vivo results in decreased nephron formation and an expanded nephrogenic precursor domain similar to that observed in Smo -deficient mutant mice. Together, our data suggest a mechanism whereby a stromal hedgehog-TGFβ2 signaling axis acts to control nephrogenesis., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2018. Published by The Company of Biologists Ltd.)