Challenges of measuring body temperatures of free-ranging birds and mammals

The thermal physiology of most birds and mammals is characterised by considerable spatial and temporal variation in body temperature. Body temperature is, therefore, a key parameter in physiological, behavioural and ecological research. Temperature measurements on freely moving or free-ranging animals in the wild are challenging but can be undertaken using a range of techniques. Internal temperature may be sampled using thermometry, surgically implanted loggers or transmitters, gastrointestinal or non-surgically placed devices. Less invasive approaches measure peripheral temperature with subcutaneous passive integrated transponder tags or skin surface-mounted radio transmitters and data loggers, or use infrared thermography to record surface temperature. Choice of technique is determined by focal research question and region of interest that reflects appropriate physiological or behavioural causal mechanisms of temperature change, as well as welfare and logistical considerations. Particularly required are further studies that provide opportunities of continuously sampling from multiple sites from within the body. This will increase our understanding of thermoregulation and temperature variation in different parts of the body and how these temperatures may change in response to physiological, behavioural and environmental parameters. Technological advances that continue to reduce the size and remote sensing capability of temperature recorders will greatly benefit field research

Applications of thermal imaging in avian science

Thermal imaging, or infrared thermography, has been used in avian science since the 1960s. More than 30 species of birds, ranging in size from passerines to ratites, have been studied using this technology. The main strength of this technique is that it is a non-invasive and non-contact method of measuring surface temperature. Its limitations and measurement errors are well understood and suitable protocols have been developed for a variety of experimental settings. Thermal imaging has been used most successfully for research on the thermal physiology of captive species, including poultry. In comparison with work on mammals, thermal imaging has been less used for population counts, other than for some large bird species. However, more recently it has shown greater success for detection of flight paths and migration. The increasing availability and reduced cost of thermal imaging systems is likely to lead to further application of this technology in studies of avian welfare, disease monitoring, energetics, behaviour and population monitoring

Water vole (Arvicola amphibius) abundance in grassland habitats of Glasgow

Water vole (Arvicola amphibius) populations have undergone a serious decline throughout the UK, and yet a stronghold of these small mammals is found in the greater Easterhouse area of Glasgow. The water voles in this location are mostly fossorial, living a largely subterranean existence in grasslands, rather than the more typical semi-aquatic lifestyle in riparian habitats. In this study, we carried out capture-mark-recapture surveys on water voles at two sites: Cranhill Park and Tillycairn Drive. We made a total of 62 captures including retraps, and the resulting population estimates were 78 individuals (95% confidence interval 41-197) for Cranhill Park and 42 individuals (20-141) for Tillycairn Drive. From these figures we estimated a population density of water voles, which appeared to be higher than other reports from the UK. Despite the difficulties of sampling in urban environments that resulted in relatively low capture rates, our data suggest that the greater Easterhouse area of Glasgow holds water voles at relatively high population densities. These results will inform future conservation in the City of Glasgow and surrounding areas, as well as raise awareness of important water vole populations in urban environments

Animal thermoregulation: a review of insulation, physiology and behaviour relevant to temperature control in buildings

Birds and mammals have evolved many thermal adaptations that are relevant to the bioinspired design of temperature control systems and energy management in buildings. Similar to many buildings, endothermic animals generate internal metabolic heat, are well insulated, regulate their temperature within set limits, modify microclimate and adjust thermal exchange with their environment. We review the major components of animal thermoregulation in endothermic birds and mammals that are pertinent to building engineering, in a world where climate is changing and reduction in energy use is needed. In animals, adjustment of insulation together with physiological and behavioural responses to changing environmental conditions fine-tune spatial and temporal regulation of body temperature, while also minimizing energy expenditure. These biological adaptations are characteristically flexible, allowing animals to alter their body temperatures to hourly, daily, or annual demands for energy. They exemplify how buildings could become more thermally reactive to meteorological fluctuations, capitalising on dynamic thermal materials and system properties. Based on this synthesis, we suggest that heat transfer modelling could be used to simulate these flexible biomimetic features and assess their success in reducing energy costs while maintaining thermal comfort for given building types

Application of phage display to high throughput antibody generation and characterization.

We have created a high quality phage display library containing over 1010 human antibodies and describe its use in the generation of antibodies on an unprecedented scale. We have selected, screened and sequenced over 38,000 recombinant antibodies to 292 antigens, yielding over 7,200 unique clones. 4,400 antibodies were characterized by specificity testing and detailed sequence analysis and the data/clones are available online. Sensitive detection was demonstrated in a bead based flow cytometry assay. Furthermore, positive staining by immunohistochemistry on tissue microarrays was found for 37% (143/381) of antibodies. Thus, we have demonstrated the potential of and illuminated the issues associated with genome-wide monoclonal antibody generation.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Regulatory Architecture of the Neuronal Cacng2/Tarpγ2 Gene Promoter: Multiple Repressive Domains, a Polymorphic Regulatory Short Tandem Repeat, and Bidirectional Organization with Co-regulated lncRNAs

CACNG2 (TARPγ2, Stargazin) is a multi-functional regulator of excitatory neurotransmission and has been implicated in the pathological processes of several brain diseases. Cacng2 function is dependent upon expression level, but currently, little is known about the molecular mechanisms that control expression of this gene. To address this deficit and investigate disease-related gene variants, we have cloned and characterized the rat Cacng2 promoter and have defined three major features: (i) multiple repressive domains that include an array of RE-1 silencing transcription factor (REST) elements, and a calcium regulatory element-binding factor (CaRF) element, (ii) a (poly-GA) short tandem repeat (STR), and (iii) bidirectional organization with expressed lncRNAs. Functional activity of the promoter was demonstrated in transfected neuronal cell lines (HT22 and PC12), but although selective removal of REST and CaRF domains was shown to enhance promoter-driven transcription, the enhanced Cacng2 promoter constructs were still about fivefold weaker than a comparable rat Synapsin-1 promoter sequence. Direct evidence of REST activity at the Cacng2 promoter was obtained through co-transfection with an established dominant-negative REST (DNR) construct. Investigation of the GA-repeat STR revealed polymorphism across both animal strains and species, and size variation was also observed in absence epilepsy disease model cohorts (Genetic Absence Epilepsy Rats, Strasbourg [GAERS] and non-epileptic control [NEC] rats). These data provide evidence of a genotype (STR)-phenotype correlation that may be unique with respect to proximal gene regulatory sequence in the demonstrated absence of other promoter, or 3′ UTR variants in GAERS rats. However, although transcriptional regulatory activity of the STR was demonstrated in further transfection studies, we did not find a GAERS vs. NEC difference, indicating that this specific STR length variation may only be relevant in the context of other (Cacna1h and Kcnk9) gene variants in this disease model. Additional studies revealed further (bidirectional) complexity at the Cacng2 promoter, and we identified novel, co-regulated, antisense rat lncRNAs that are paired with Cacng2 mRNA. These studies have provided novel insights into the organization of a synaptic protein gene promoter, describing multiple repressive and modulatory domains that can mediate diverse regulatory inputs

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease