Wichmannscott3259

Cat scratch disease (CSD) in humans is caused by infection with Bartonella henselae or other Bartonella spp. The name of the disease reflects the fact that patients frequently have a history of contact (often involving bites or scratches) with infected cats. Patients with CSD typically develop lesions at the site where the skin is broken together with regional lymphadenopathy but may go on to exhibit systemic symptoms and with deep-seated infections at a range of sites including the eye. Patients with CSD may present with a range of inflammatory eye conditions, including Parinaud's oculoglandular syndrome, neuroretinitis, multifocal retinitis, uveitis and retinal artery occlusion. Bartonella spp. are fastidious bacteria that are difficult to culture from clinical specimens so microbiological diagnosis is frequently made on the basis of positive serology for anti-Bartonella antibodies or detection of bacterial DNA by PCR. Due to the lack of clinical trials, the evidence base for optimal management of patients with CSD-associated eye infections (including the role of antibiotics) is weak, being derived from single reports or small, uncontrolled case series. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.AIMS To characterise posterior corneal surface features in patients with Down syndrome (DS) and to compare them with healthy and mild keratoconus corneas. METHODS This restrospective, comparative, non-randomised, clinical study included 123 eyes, divided into three groups (37 eyes of patients with DS, 46 with mild keratoconus and 40 controls), and took place at Vissum Alicante. Only patients with no previous ocular surgery, no corneal scars and no active ocular disease other than keratoconus were included. The Sirius System topographer (CSO, Firenze, Italy) was used in order to analyse posterior corneal surface keratometry, shape and keratoconus screening indices, posterior corneal aberrations, corneal volume and pachymetry. RESULTS Patients with DS, when compared with healthy controls, have a steeper (mean keratometry 7 mm (KM) -6.30±0.44 vs -6.15±0.22; p0.05) in KM (-6.38±0.34), HOA (0.56±0.36), coma-like (0.51±0.34) and pachymetry (500.56±36.83). CONCLUSIONS Posterior corneal surface of patients with DS is steeper, more irregular and shows more higher order aberrations, as well as reduced volume and thinner pachymetry than patients with healthy corneas. Additionally, posterior corneal surface in patients with DS shows similar characteristics to those found in mild keratoconus. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.AIMS To investigate the effect of fundus tracking perimetry on structure-function relationship in glaucoma. METHODS Perimetric data were acquired with the Humphrey Field Analyzer (HFA) and the Compass fundus perimeter (CMP, equipped with fundus tracking). We included data from 696 eyes from 360 healthy people and 711 eyes from 434 patients with glaucoma from the original study, for which the circumpapillary retinal nerve fibre layer optical coherence tomography scan (Cp-RNFL) was available. We explored the structure-function relationship using both global indices (mean deviation and average Cp-RNFL thickness loss) and anatomically defined visual field clusters comparing the R2 values from mixed-effect models. We then measured the diagnostic ability of a combined Structure Function Index (SFI) using perimetric data from either perimeter. The comparisons were based on partial receiver operating characteristic curves with a minimum specificity of 75% and their areas under the curve. RESULTS The R2 for the global structure-function relationship was 0.50 for the CMP and 0.48 for the HFA. When visual field clusters were included in the model, the R2 was 0.29 for CMP and 0.30 for HFA. Overall, the discrimination ability of the SFI was not significantly higher than the Cp-RNFL for either the CMP (p=0.07) or the HFA (p=0.14). However, it was significantly better in eyes with perimetric damage (p less then 0.001), in which the CMP-SFI performed significantly better than the HFA-SFI (p=0.03). CONCLUSIONS Structure-function relationship is similar between the two perimeters. Cell Cycle inhibitor Fundus tracking might improve discrimination ability with a combined SFI. TRIAL REGISTRATION NUMBER ISRCTN13800424. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.Sally Lowell is a Wellcome Trust Senior Research Fellow at the University of Edinburgh, UK. Her research group, which is based in the Centre for Regenerative Medicine, studies cell fate decisions in stem cells, focussing on how communication and interactions between cells can influence these decisions. Sally, who has been a long-serving committee member of the British Society for Developmental Biology, recently joined the Board of Directors at The Company of Biologists. We caught up with Sally to find out more about her career and her research, and why she's excited about her role at the Company. © 2020. Published by The Company of Biologists Ltd.Mutations in the Ultrabithorax (Ubx) gene cause homeotic transformation of the normally two-winged Drosophila into a four-winged mutant fly. Ubx encodes a HOX family transcription factor that specifies segment identity, including transformation of the second set of wings into rudimentary halteres. Ubx is known to control the expression of many genes that regulate tissue growth and patterning, but how it regulates tissue morphogenesis to reshape the wing into a haltere is still unclear. Here, we show that Ubx acts by repressing the expression of two genes in the haltere, Stubble and Notopleural, both of which encode transmembrane proteases that remodel the apical extracellular matrix to promote wing morphogenesis. In addition, Ubx induces expression of the Tissue inhibitor of metalloproteases in the haltere, which prevents the basal extracellular matrix remodelling necessary for wing morphogenesis. Our results provide a long-awaited explanation for how Ubx controls morphogenetic transformation. © 2020. Published by The Company of Biologists Ltd.