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In this study, propensity score matching (PSM) was conducted to examine differences in the effectiveness of research mentor training (RMT) implemented using two modes--face-to-face or synchronous online training. This study investigated each training mode and assessed participants' perceived gains in mentoring skills, ability to meet mentees' expectations, and overall quality of mentoring, as well as intention to make changes to their mentoring practices. Additional factors that may contribute to participant outcomes were also examined. In total, 152 mentors trained using a synchronous online platform and 655 mentors trained in in-person workshops were analyzed using the PSM method. Mentors were matched based on similar characteristics, including mentee's career stage, mentor's title, mentor's prior mentoring experience, mentor's race/ethnicity and sex, and mentor's years of experience; results show that both face-to-face and synchronous online modes of RMT are effective. Findings indicated that the training mode did not significantly impact the mentors' perceived training outcomes. Factors associated with the reported training outcomes included dosage (hours of training), facilitator effectiveness, race/ethnicity, and previous mentoring experience. The results of this study demonstrate that mentors' perceived training outcomes are comparable regardless of the training modality used--online versus face-to-face.

BackgroundOur objective is to better comprehend treatment considerations for urethral stricture disease (USD) in patients requiring long-term clean intermittent catheterization (CIC). Patient characteristics, surgical outcomes and complications are unknown in this population.MethodsSix members of the Trauma and Urologic Reconstruction Network of Surgeons (TURNS) participated in a prospective (2009 to present) and retrospective (prior to 2009) database recording patient demographics, surgical approach and outcomes. We included all patients undergoing urethroplasty who perform CIC. Descriptive statistics were used to analyze results.ResultsA total of 37 patients with 39 strictures were included. Bladder dysfunction was characterized as detrusor failure in 35% and neurogenic etiology in 65%. Median stricture length was 3 cm (IQR: 1.5-5.5) with 28% repaired with dorsal onlay buccal mucosal graft, 26% excision and primary anastomosis, 8% dorsal inlay, 8% ventral and dorsal, 8% flap based 8% non-transecting and 15% other. Functional success was 90%: 4 patients required DVIU or dilation due to recurrence, with 2 of those ultimately requiring repeat urethroplasty. 86% of patients returned to CIC; no patients reported new pad use for urinary leakage after urethroplasty. During a median follow-up period of 3.1 years (IQR: 1.0-5.3), no patients underwent urinary diversion.ConclusionsUrethroplasty is suitable, safe and effective for patients dependent on CIC suffering from USD. The effect of continual CIC on long-term outcomes remains uncertain.

ObjectiveA high level of vascular endothelial growth factor (VEGF) has been implicated in brain arteriovenous malformation (bAVM) bleeding and rupture. However, direct evidence is missing. In this study the authors used a mouse bAVM model to test the hypothesis that elevation of focal VEGF levels in bAVMs exacerbates the severity of bAVM hemorrhage.MethodsBrain AVMs were induced in adult mice in which activin receptor-like kinase 1 (Alk1, a gene that causes AVM) gene exons 4-6 were floxed by intrabasal ganglia injection of an adenoviral vector expressing Cre recombinase to induce Alk1 mutation and an adeno-associated viral vector expressing human VEGF (AAV-VEGF) to induce angiogenesis. Two doses of AAV-VEGF (5 × 109 [high] or 2 × 109 [low]) viral genomes were used. In addition, the common carotid artery and external jugular vein were anastomosed in a group of mice treated with low-dose AAV-VEGF 6 weeks after the model induction to induce cerebral venous hypertension (VH), because VH increases the VEGF level in the brain. Brain samples were collected 8 weeks after the model induction. Hemorrhages in the bAVM lesions were quantified on brain sections stained with Prussian blue, which detects iron deposition. VEGF levels were quantified in bAVM tissue by enzyme-linked immunosorbent assay.ResultsCompared to mice injected with a low dose of AAV-VEGF, the mice injected with a high dose had higher levels of VEGF (p = 0.003) and larger Prussian blue-positive areas in the bAVM lesion at 8 or 9 weeks after model induction (p = 0.002). VH increased bAVM hemorrhage in the low-dose AAV-VEGF group. The overall mortality in the high-dose AAV-VEGF group was 26.7%, whereas no mouse died in the low-dose AAV-VEGF group without VH. In contrast, VH caused a mortality of 50% in the low-dose AAV-VEGF group.ConclusionsUsing mouse bAVM models, the authors provided direct evidence that elevation of the VEGF level increases bAVM hemorrhage and mouse mortality.

ObjectiveA high level of vascular endothelial growth factor (VEGF) has been implicated in brain arteriovenous malformation (bAVM) bleeding and rupture. However, direct evidence is missing. In this study the authors used a mouse bAVM model to test the hypothesis that elevation of focal VEGF levels in bAVMs exacerbates the severity of bAVM hemorrhage.MethodsBrain AVMs were induced in adult mice in which activin receptor-like kinase 1 (Alk1, a gene that causes AVM) gene exons 4-6 were floxed by intrabasal ganglia injection of an adenoviral vector expressing Cre recombinase to induce Alk1 mutation and an adeno-associated viral vector expressing human VEGF (AAV-VEGF) to induce angiogenesis. Two doses of AAV-VEGF (5 × 109 [high] or 2 × 109 [low]) viral genomes were used. In addition, the common carotid artery and external jugular vein were anastomosed in a group of mice treated with low-dose AAV-VEGF 6 weeks after the model induction to induce cerebral venous hypertension (VH), because VH increases the VEGF level in the brain. Brain samples were collected 8 weeks after the model induction. Hemorrhages in the bAVM lesions were quantified on brain sections stained with Prussian blue, which detects iron deposition. VEGF levels were quantified in bAVM tissue by enzyme-linked immunosorbent assay.ResultsCompared to mice injected with a low dose of AAV-VEGF, the mice injected with a high dose had higher levels of VEGF (p = 0.003) and larger Prussian blue-positive areas in the bAVM lesion at 8 or 9 weeks after model induction (p = 0.002). VH increased bAVM hemorrhage in the low-dose AAV-VEGF group. The overall mortality in the high-dose AAV-VEGF group was 26.7%, whereas no mouse died in the low-dose AAV-VEGF group without VH. In contrast, VH caused a mortality of 50% in the low-dose AAV-VEGF group.ConclusionsUsing mouse bAVM models, the authors provided direct evidence that elevation of the VEGF level increases bAVM hemorrhage and mouse mortality.

Summary: Treating insomnia during pregnancy improves sleep and depressed mood. However, given well‐established links between poor sleep and a broad spectrum of adverse maternal outcomes, the benefits of insomnia care may reach beyond sleep and depression. The present study evaluated the preliminary efficacy of 'Perinatal Understanding of Mindful Awareness for Sleep' (PUMAS)—a mindfulness sleep programme tailored to pregnancy that combines behavioural sleep strategies and meditation—for enhancing everyday mindfulness and maternal–fetal attachment, as well as for alleviating anxiety, repetitive thinking, and sleep‐related daytime impairment. We conducted a secondary analysis of a single‐arm proof‐of‐concept trial of 11 pregnant women with fifth edition of the Diagnostic and Statistical Manual of Mental Disorders diagnosed insomnia disorder who completed PUMAS (six sessions), which was delivered in an individual format via telemedicine video. Pre‐ and post‐treatment outcomes included the Cognitive and Affective Mindfulness Scale‐Revised (CAMS‐R), Maternal–Fetal Attachment Scale (MFAS), Generalised Anxiety Disorder seven‐item survey (GAD‐7), Perseverative Thinking Questionnaire (PTQ), Daytime Insomnia Symptoms Response Scale (DISRS), and the Patient‐Reported Outcomes Measurement Information System Sleep‐Related Impairment Scale (PROMIS‐SRI). Symptom changes were evaluated with paired‐samples t tests. Results showed PUMAS patients reported large increases in CAMS‐R (Cohen's dz = 1.81) and medium‐large increases in MFAS scores (Cohen's dz = 0.73). Moreover, PUMAS patients reported large reductions in scores on the GAD‐7 (Cohen's dz = 1.09), PTQ (Cohen's dz = 1.26), DISRS (Cohen's dz = 1.38), and PROMIS‐SRI (Cohen's dz = 1.53). Preliminary evidence suggests that a mindfulness‐based perinatal sleep programme may benefit several domains of maternal wellbeing beyond sleep and depression. PUMAS substantially enhanced patient ratings of everyday mindfulness and maternal–fetal attachment, while reporting alleviations in anxiety, perseverative thinking, insomnia‐focused rumination, and sleep‐related daytime impairment. [ABSTRACT FROM AUTHOR]

Several laboratories have carried out molecular dynamics (MD) simulations of arginine interactions with lipid bilayers and found that the energetic cost of placing arginine in lipid bilayers is an order of magnitude greater than observed in molecular biology experiments in which Arg-containing transmembrane helices are inserted across the endoplasmic reticulum membrane by the Sec61 translocon. We attempt here to reconcile the results of the two approaches. We first present MD simulations of guanidinium groups alone in lipid bilayers, and then, to mimic the molecular biology experiments, we present simulations of hydrophobic helices containing single Arg residues at different positions along the helix. We discuss the simulation results in the context of molecular biology results and show that the energetic discrepancy is reduced, but not eliminated, by considering free energy differences between Arg at the interface and at the center of the model helices. The reduction occurs because Arg snorkeling to the interface prevents Arg from residing in the bilayer center where the energetic cost of desolvation is highest. We then show that the problem with MD simulations is that they measure water-to-bilayer free energies, whereas the molecular biology experiments measure the energetics of partitioning from translocon to bilayer, which raises the fundamental question of the relationship between water-to-bilayer and water-to-translocon partitioning. We present two thermodynamic scenarios as a foundation for reconciliation of the simulation and molecular biology results. The simplest scenario is that translocon-to-bilayer partitioning is independent of water-to-bilayer partitioning; there is no thermodynamic cycle connecting the two paths.