Matthew Baillie's specimens and engravings

In 1799, Matthew Baillie, William Hunter's nephew, published his famous atlas of pathology. It was entitled A Series of Engravings Accompanied with Explanations which are Intended to Illustrate the Morbid Anatomy of Some of the Most Important Parts of the Human Body. The present study aims to match the illustrations to extant specimens in the collections of William and John Hunter, preserved at the University of Glasgow and at the Royal College of Surgeons of England respectively. Baillie's book contains 10 fasciculi, consisting of 73 plates and 206 figures. The specimens Baillie illustrated came from his own collection and those of ten others, including his uncles, William and John Hunter. The book was illustrated by William Clift and engraved by James Basire, William Skelton and James Heath. Excluding eight illustrations of intestinal worms where the provenance of the specimens is uncertain, a total of 98 specimens from William Hunter's collection were illustrated in 104 figures. Eight of the specimens were calculi impossible to identify specifically. Excluding worms and calculi, 72 of William Hunter's specimens illustrated by Baillie are extant in the Hunterian Collection at the University of Glasgow. All but one of the 20 specimens illustrated that had belonged to John Hunter were identified in the on-line catalogue of the Royal College of Surgeons of England. Baillie's own collection was destroyed when the Royal College of Surgeons of England was bombed in 1941. Baillie is credited with being the first to produce an illustrated systematic textbook of morbid anatomy and probably the first to illustrate emphysema and transposition of the great vessels. His book, however, was not comprehensive. It did not cover a number of topics such as muscles and bones and there is little coverage of the nervous system. Baillie's book, however, was an original concept as an atlas of morbid anatomy and showed his deep insight into pathology

Give me a break! Unavoidable fatigue effects in cognitive pupillometry

Issue Online: 08 June 2023Pupillometry has a rich history in the study of perception and cognition. One perennial challenge is that the magnitude of the task-evoked pupil response diminishes over the course of an experiment, a phenomenon we refer to as a fatigue effect. Reducing fatigue effects may improve sensitivity to task effects and reduce the likelihood of confounds due to systematic physiological changes over time. In this paper, we investigated the degree to which fatigue effects could be ameliorated by experimenter intervention. In Experiment 1, we assigned participants to one of three groups—no breaks, kinetic breaks (playing with toys, but no social interaction), or chatting with a research assistant—and compared the pupil response across conditions. In Experiment 2, we additionally tested the effect of researcher observation. Only breaks including social interaction significantly reduced the fatigue of the pupil response across trials. However, in all conditions we found robust evidence for fatigue effects: that is, regardless of protocol, the task-evoked pupil response was substantially diminished (at least 60%) over the duration of the experiment. We account for the variance of fatigue effects in our pupillometry data using multiple common statistical modeling approaches (e.g., linear mixed-effects models of peak, mean, and baseline pupil diameters, as well as growth curve models of time-course data). We conclude that pupil attenuation is a predictable phenomenon that should be accommodated in our experimental designs and statistical models.Agencia Estatal de Investigación, Grant/Award Number: CEX2020-001010- S; Eusko Jaurlaritza; National Institutes of Health, Grant/ Award Number: R01 DC014281 and R01 DC019507; National Science Foundation, Grant/Award Number: DGE-174503

Rare and low-frequency coding variants alter human adult height

Height is a highly heritable, classic polygenic trait with ~700 common associated variants identified so far through genome - wide association studies . Here , we report 83 height - associated coding variants with lower minor allele frequenc ies ( range of 0.1 - 4.8% ) and effects of up to 2 16 cm /allele ( e.g. in IHH , STC2 , AR and CRISPLD2 ) , >10 times the average effect of common variants . In functional follow - up studies, rare height - increasing alleles of STC2 (+1 - 2 cm/allele) compromise d proteolytic inhibition of PAPP - A and increased cleavage of IGFBP - 4 in vitro , resulting in higher bioavailability of insulin - like growth factors . The se 83 height - associated variants overlap genes mutated in monogenic growth disorders and highlight new biological candidates ( e.g. ADAMTS3, IL11RA, NOX4 ) and pathways ( e.g . proteoglycan/ glycosaminoglycan synthesis ) involved in growth . Our results demonstrate that sufficiently large sample sizes can uncover rare and low - frequency variants of moderate to large effect associated with polygenic human phenotypes , and that these variants implicate relevant genes and pathways

Genomic investigations of unexplained acute hepatitis in children

Since its first identification in Scotland, over 1,000 cases of unexplained paediatric hepatitis in children have been reported worldwide, including 278 cases in the UK1. Here we report an investigation of 38 cases, 66 age-matched immunocompetent controls and 21 immunocompromised comparator participants, using a combination of genomic, transcriptomic, proteomic and immunohistochemical methods. We detected high levels of adeno-associated virus 2 (AAV2) DNA in the liver, blood, plasma or stool from 27 of 28 cases. We found low levels of adenovirus (HAdV) and human herpesvirus 6B (HHV-6B) in 23 of 31 and 16 of 23, respectively, of the cases tested. By contrast, AAV2 was infrequently detected and at low titre in the blood or the liver from control children with HAdV, even when profoundly immunosuppressed. AAV2, HAdV and HHV-6 phylogeny excluded the emergence of novel strains in cases. Histological analyses of explanted livers showed enrichment for T cells and B lineage cells. Proteomic comparison of liver tissue from cases and healthy controls identified increased expression of HLA class 2, immunoglobulin variable regions and complement proteins. HAdV and AAV2 proteins were not detected in the livers. Instead, we identified AAV2 DNA complexes reflecting both HAdV-mediated and HHV-6B-mediated replication. We hypothesize that high levels of abnormal AAV2 replication products aided by HAdV and, in severe cases, HHV-6B may have triggered immune-mediated hepatic disease in genetically and immunologically predisposed children

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

The cautionary tale of Lister\u27s stromb

Volume: 23Start Page: 9End Page: 1

Bird nests in museum collections: a rich resource for research

Data-rich birds' nests in museum collections are relatively rarely used in ornithological research but can be valuable sources of scientific data. Materials, architecture, artefacts of utilisation and preserved nest fauna all combine to make museum nest collections potentially excellent behavioural archives. Over recent years, the Natural History Museum, Tring, and the Hunterian Museum, Glasgow, have cooperatively developed their respective collections to deliver a combined research resource that is international in scope, increasingly taxonomically representative and rich in time-series of nest specimens for British breeding species. Here we review the role of museum nest collections in furthering avian research and explore how new research techniques may potentially provide exciting opportunities. We also consider collection development and how collections might be better tailored to the needs of avian biology researchers