What matters in mental health care? A co-design approach to developing clinical supervision tools for practitioner competency development

Abstract Background Specialised mental health (MH) care providers are often absent or scarcely available in low resource and humanitarian settings (LRHS), making MH training and supervision for general health care workers (using task-sharing approaches) essential to scaling up services and reducing the treatment gap for severe and common MH conditions. Yet, the diversity of settings, population types, and professional skills in crisis contexts complicate these efforts. A standardised, field tested instrument for clinical supervision would be a significant step towards attaining quality standards in MH care worldwide. Methods A competency-based clinical supervision tool was designed by Médecins Sans Frontières (MSF) for use in LRHS. A systematic literature review informed its design and assured its focus on key clinical competencies. An initial pool of behavioural indicators was identified through a rational theoretical scale construction approach, tested through waves of simulation and reviewed by 12 MH supervisors in seven projects where MSF provides care for severe and common MH conditions. Results Qualitative analysis yielded two sets of competency grids based on a supervisee's professional background: one for ‘psychological/counselling’ and another for ‘psychiatric/mhGAP’ practitioners. Each grid features 22–26 competencies, plus optional items for specific interventions. While the structure and content were assessed as logical by supervisors, there were concerns regarding the adequacy of the tool to field reality. Conclusions Humanitarian settings have specific needs that require careful consideration when developing capacity-building strategies. Clinical supervision of key competencies through a standardised instrument represents an important step towards ensuring progress of clinical skills among MH practitioners

Hemorrhage rate after coblation tonsillectomy: a meta-analysis of published trials

After the surgical procedure of tonsillectomy, hemorrhage ranks among its serious postoperative complications. In this systematic review, we analyze hemorrhage following tonsillectomies performed using the coblation technique. 24 prospective, randomized, and controlled studies were included in the meta-analysis. Data of 796 patients who had undergone coblation tonsillectomy were analyzed. Hemorrhages occurred in 33 patients: 2 classified as primary and 26 as secondary hemorrhages. 5 could not be classified into either group. Overall, the total hemorrhage rate for the coblation procedure was 4.1% with a 95% confidence interval from 2.8 to 5.5%. The overall hemorrhage rate of 4.1% found in this meta-analysis shows that coblation is a safe and effective technique for tonsillectomies with a secondary bleeding rate similar to what is reported for comparable techniques such as bipolar diathermia

Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure.

Numerous genetic loci have been associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Europeans. We now report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP). In discovery (N = 74,064) and follow-up studies (N = 48,607), we identified at genome-wide significance (P = 2.7 × 10(-8) to P = 2.3 × 10(-13)) four new PP loci (at 4q12 near CHIC2, 7q22.3 near PIK3CG, 8q24.12 in NOV and 11q24.3 near ADAMTS8), two new MAP loci (3p21.31 in MAP4 and 10q25.3 near ADRB1) and one locus associated with both of these traits (2q24.3 near FIGN) that has also recently been associated with SBP in east Asians. For three of the new PP loci, the estimated effect for SBP was opposite of that for DBP, in contrast to the majority of common SBP- and DBP-associated variants, which show concordant effects on both traits. These findings suggest new genetic pathways underlying blood pressure variation, some of which may differentially influence SBP and DBP

Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.

Blood pressure is a heritable trait influenced by several biological pathways and responsive to environmental stimuli. Over one billion people worldwide have hypertension (≥140 mm Hg systolic blood pressure or  ≥90 mm Hg diastolic blood pressure). Even small increments in blood pressure are associated with an increased risk of cardiovascular events. This genome-wide association study of systolic and diastolic blood pressure, which used a multi-stage design in 200,000 individuals of European descent, identified sixteen novel loci: six of these loci contain genes previously known or suspected to regulate blood pressure (GUCY1A3-GUCY1B3, NPR3-C5orf23, ADM, FURIN-FES, GOSR2, GNAS-EDN3); the other ten provide new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke and coronary artery disease, but not kidney disease or kidney function. We also observed associations with blood pressure in East Asian, South Asian and African ancestry individuals. Our findings provide new insights into the genetics and biology of blood pressure, and suggest potential novel therapeutic pathways for cardiovascular disease prevention

Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function.

Reduced glomerular filtration rate defines chronic kidney disease and is associated with cardiovascular and all-cause mortality. We conducted a meta-analysis of genome-wide association studies for estimated glomerular filtration rate (eGFR), combining data across 133,413 individuals with replication in up to 42,166 individuals. We identify 24 new and confirm 29 previously identified loci. Of these 53 loci, 19 associate with eGFR among individuals with diabetes. Using bioinformatics, we show that identified genes at eGFR loci are enriched for expression in kidney tissues and in pathways relevant for kidney development and transmembrane transporter activity, kidney structure, and regulation of glucose metabolism. Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues demonstrate preferential mapping of associated variants to regulatory regions in kidney but not extra-renal tissues. These findings suggest that genetic determinants of eGFR are mediated largely through direct effects within the kidney and highlight important cell types and biological pathways

Liposomal Nasal Spray versus Guideline-Recommended Steroid Nasal Spray in Patients with Chronic Rhinosinusitis: A Comparison of Tolerability and Quality of Life

Objective. To investigate the tolerability and impact on quality of life of liposomal nasal spray compared to guideline-recommended steroid-based therapy in patients with chronic rhinosinusitis. Symptom reduction and use of antisymptomatic medication were also examined. Methods. In this monocenter, prospective, controlled, open, and noninterventional study, 60 patients with chronic rhinosinusitis were treated with liposomal nasal spray and 30 patients received steroid-based therapy. The study comprised five visits occurring at intervals of two to four weeks. Efficacy was determined according to the sinusitis symptom score documented daily. The polyp score was recorded at the initial and final visits. Tolerability was determined through the Nasal Spray Evaluation Questionnaire, and quality of life was ascertained with the SNOT-20 Score. Results. Both treatments achieved a significant reduction of sinusitis symptoms (P<0.05) and also rhinoscopic improvement (P<0.05). The majority of patients assessed the treatments as “good” or “very good,” and the quality of life improved significantly (P<0.05). There was no significant difference in symptom reduction, QoL, and endoscopic exams between both treatments. Conclusion. The treatment of chronic rhinosinusitis with liposomal nasal spray results in a similar, significant reduction of symptoms and significant improvement in quality of life as guideline-recommended treatment and is therefore a comparable alternative

Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Niemann-Pick c1-like 1

International audienceCholesterol membrane transporters [scavenger receptor class B type I (SR-BI) and (cluster determinant 36) are involved in intestinal uptake of lutein and β-carotene, 2 of the 3 main carotenoids of the human diet. The aim of this work was therefore to determine whether SR-BI and NPC1L1 (Niemann-Pick C1-like 1), another cholesterol transporter, are implicated in absorption of lycopene, the 3rd main carotenoid of the human diet. Anti-human SR-BI antibody and block lipid transport 1 (BLT1) (a chemical inhibitor of lipid transport by SR-BI) impaired up to 60% (all-E) and (5Z)-lycopene uptake (P < 0.05) by Caco-2 cell monolayers, which were used as a model of human intestinal epithelium. The involvement of SR-BI in lycopene absorption in vivo was then verified by comparing plasma lycopene concentrations in wild-type and SR-BI transgenic mice that were fed a diet enriched with 0.25 g/kg (all-E)-lycopene for 1 mo. Plasma lycopene concentrations were ~10-fold higher (P < 0.001) in mice overexpressing SR-BI in the intestine than in wild-type mice, confirming the involvement of SR-BI in lycopene absorption. Further experiments showed that (all-E)-lycopene did not affect SR-BI mRNA levels in Caco-2 cells or mouse intestine. In contrast to SR-BI, neither anti-human NPC1L1 antibody nor ezetimibe, used as inhibitors of lycopene uptake via NPC1L1, significantly impaired (all-E) or (5Z)-lycopene uptake by Caco-2 monolayers. Thus, the present data show that lycopene absorption is, at least in part, mediated by SR-BI but not by NPC1L

Increased Corneal Endothelial Cell Migration in Fuchs Endothelial Corneal Dystrophy

Purpose: To investigate if corneal endothelial cells (CECs) in Fuchs endothelial corneal dystrophy (FECD) have altered cellular migration compared with normal controls. Design: Comparative analysis. Materials: Descemet’s membrane and CECs derived from patients with FECD undergoing endothelial keratoplasty or normal cadaveric donors. Methods: Ex vivo specimens were used for live cell imaging and generation of immortalized cell lines. Live imaging was performed on FECD and normal CECs and on ex vivo specimens transfected with green fluorescent protein. Migration speeds were determined as a function of cellular density using automated cell tracking. Ex vivo specimens were classified as either FECD or normal low cell density (nonconfluent) or high cell density (confluent). Scratch assay was performed on CECs seeded at high confluence to determine migration speed. Genetic analysis from blood samples or CECs was performed to detect a CTG repeat expansion in the TCF4 gene. Main Outcome Measures: Mean cell migration speed. Results: Fuchs endothelial corneal dystrophy CECs in low cell density areas displayed increased mean speed (0.391 ± 0.005 μm/minute vs. 0.364 ± 0.005 μm/minute; P < 0.001) and mean maximum speed (0.961 ± 0.010 μm/minute vs. 0.787 ± 0.011 μm/minute; P < 0.001) compared with normal CECs, and increased mean maximum speed (0.778 ± 0.014 μm/minute vs. 0.680 ± 0.011 μm/minute; P < 0.001) in high cell density areas ex vivo. Similarly, FECD CECs displayed increased mean speed compared with normal CECs (1.958 ± 0.020 μm/minute vs. 2.227 ± 0.021 μm/minute vs. 1.567 ± 0.019 μm/minute; P < 0.001) under nonconfluent conditions in vitro. Moreover, FECD CECs also displayed increased mean speed compared with normal CECs under high confluent conditions as detected by scratch assay (37.2 ± 1.1% vs. 44.3 ± 4.1% vs. 70.7 ± 5.2%; P < 0.001). Morphologic analysis showed that FECD CECs displayed an increased fibroblastic phenotype as detected by filamentous-actin labeling. Conclusions: Fuchs endothelial corneal dystrophy CECs demonstrated increased migration speed compared with normal CECs. Further investigation into the mechanisms of heightened cell migration in FECD is needed and may provide insight into its pathogenesis, as well as having implications on descemetorhexis without endothelial keratoplasty