Investigating Collaborative Data Practices: a Case Study on Artificial Intelligence for Healthcare Research

Developing artificial intelligence (AI) tools for healthcare is a collaborative effort, bringing data scientists, clinicians, patients and other disciplines together. In this paper, we explore the collaborative data practices of research consortia tasked with applying AI tools to understand and manage multiple long-term conditions in the UK. Through an inductive thematic analysis of 13 semi-structured interviews with participants of these consortia, we aimed to understand how collaboration happens based on the tools used, communication processes and settings, as well as the conditions and obstacles for collaborative work. Our findings reveal the adaptation of tools that are used for sharing knowledge and the tailoring of information based on the audience, particularly those from a clinical or patient perspective. Limitations on the ability to do this were also found to be imposed by the use of electronic healthcare records and access to datasets. We identified meetings as the key setting for facilitating exchanges between disciplines and allowing for the blending and creation of knowledge. Finally, we bring to light the conditions needed to facilitate collaboration and discuss how some of the challenges may be navigated in future work.Comment: 17 page

Determining the Minimum Inhibitory Concentration of Medium Chain Fatty Acids for Generic Escherichia coli, Enterotoxigenic Escherichia coli, Salmonella Typhimurium, and Campylobacter coli

Research has demonstrated that medium chain fatty acids (MCFA) can serve as reduction strategies for bacterial and viral pathogens in animal feed and ingredients. However, it is unknown how the type or level of MCFA impact bacteria growth. This can be tested through a minimum inhibitory concentration (MIC) benchtop assay, which identifies the lowest concentration of a chemical that prevents visible growth of a bacterium. The objective of this study was to 1) determine the MCFA MIC of C6:0, C8:0, C10:0, and C12:0 for genericEscherichiacoli, EnterotoxigenicEscherichia coli,SalmonellaTyphimurium,Campylobactercoli, andClostridium perfringens; 2) determine the MIC of commercial based MCFA products against the same bacteria; and 3) determine the effect of 2 commercial based MCFA products on the quantification of EnterotoxigenicEscherichia coli. For Exp. 1 and 2, MIC were determined by modified microbroth dilution method using a 96 well microtiter plate with a concentration of 105 CFU/mL for each bacterial strain. For Exp. 3, the two products selected for quantification were mixed with a complete swine diet and inoculated with two concentrations (106 or 102 CFU/g of feed) of aNalRstrain of EnterotoxigenicEscherichia coli(ETEC) for bacterial enumeration. From Exp. 1, the MIC of MCFA varied among bacteria species. The lowest MIC of the MCFA was 0.43% of a 1:1:1 blend of C6:0, C8:0, and C10:0 forCampylobacter coli, 0.25% C12:0 forClostridium perfringens, 0.60% 1:1:1 blend for genericEscherichia coli, 0.53% C6:0 for ETEC, and 0.40% C6:0 forSalmonellaTyphimurium. In Exp. 2, products containing high concentrations of C6:0 or C8:0 had lower MIC in gram negative bacteria. In Exp. 3, feed containing either of the commercial based MCFA products reduced (linear,P\u3c0.05) quantifiable ETEC. Overall, the inhibitory efficacy of MCFA varies among bacteria species. This suggests that MCFA mixtures may provide a wider spectrum of bacterial control. As commercial products containing MCFA become available for livestock, it is important to consider the interaction between MCFA chain length and concentration on the potential to effectively mitigate various feed-based bacteria

Effects of Tylosin Administration Routes on the Development of Antimicrobial Resistance in Fecal Enterococci of Finishing Swine

Antibiotics can be administered via various routes in pigs, which may influence antimicrobial resistance development. A total of 40 barrows and 40 gilts (Line 600 × 241; DNA, Columbus, NE; initially 207 ± 7.9 lb) were used in a 35-d trial to determine the effects of tylosin administration route on pig growth performance and development of antimicrobial resistance in fecal Enterococcus spp. isolates. Pens of pigs (1 pig/ pen, 20 pigs/treatment) were blocked by initial body weight (BW) and gender. Within blocks, pens were randomly allotted to 1 of 4 treatments. The antibiotic treatments followed US label directions and were: 1) no antibiotic (Control); 2) 110 mg tylosin per kg of feed for 21 d (Feed); 3) 8.82 mg tylosin per kg of BW through intramuscular injection twice daily for the first 3 d of each wk during the 3-wk treatment period (Injection); and 4) 66 mg of tylosin per liter of drinking water for the first 3 d of each wk during treatment period (Water). Treatments were offered during d 0 to 21, after which all pigs were fed a common diet with no antibiotic until d 35. Fecal samples were collected on d 0, 21, and 35. No evidence for route × gender interactions (P \u3e 0.55) were observed for any growth responses. From d 0 to 21, control pigs and pigs fed medicated feed had greater (P \u3c 0.05) average daily gain (ADG) than those that received injected tylosin, with the ADG of pigs receiving tylosin through the water intermediate. There was no evidence for different average daily feed intake (ADFI) among treatment groups. Pigs that received tylosin through injection or water had poorer (P \u3c 0.05) feed efficiency (F/G) compared with control pigs, but there was no evidence for difference from pigs receiving tylosin through feed. Among the medicated pigs, total tylosin dose administered was the greatest through injection, second highest through feed, with the water medication route the lowest. No evidence for route × day interactions (P \u3e 0.23) were observed for the development of bacterial resistance to any antibiotics. Enterococcal isolates collected from pigs receiving tylosin via feed or injection were more resistant (P \u3c 0.05) to erythromycin and tylosin compared with control pigs and those that received tylosin through water. The estimated probability of antimicrobial resistance to these 2 antibiotics was greater on d 21 and 35 than d 0. In summary, tylosin injection resulted in poorer ADG and F/G of finishing pigs, likely due to stress associated with handling and injection. Tylosin administration through injection and feed resulted in greater probability of enterococcal resistance to erythromycin and tylosin compared with in-water treatment, which is likely a combined effect of administration route and dosage

Long-term air pollution exposure and Parkinson's disease mortality in a large pooled European cohort: An ELAPSE study

BACKGROUND: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson's Disease (PD) remains limited. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts. METHODS: Within the project 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (O3), as well as 8 PM2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders. RESULTS: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM2.5 (hazard ratio per 5 µg/m3: 1.25; 95% confidence interval: 1.01-1.55), NO2 (1.13; 0.95-1.34 per 10 µg/m3), and BC (1.12; 0.94-1.34 per 0.5 × 10-5m-1), and a negative association with O3 (0.74; 0.58-0.94 per 10 µg/m3). Associations of PM2.5, NO2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM2.5 remained robust when adjusted for NO2 (1.24; 0.95-1.62) or BC (1.28; 0.96-1.71), whereas associations with NO2 or BC attenuated to null. O3 associations remained negative, but no longer statistically significant in models with PM2.5. We detected suggestive positive associations with the potassium component of PM2.5. CONCLUSION: Long-term exposure to PM2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality

Long-term air pollution exposure and Parkinson's disease mortality in a large pooled European cohort: An ELAPSE study

BACKGROUND: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson's Disease (PD) remains limited. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts. METHODS: Within the project 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM 2.5), nitrogen dioxide (NO 2), black carbon (BC), and ozone (O 3), as well as 8 PM 2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders. RESULTS: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM 2.5 (hazard ratio per 5 µg/m 3: 1.25; 95% confidence interval: 1.01-1.55), NO 2 (1.13; 0.95-1.34 per 10 µg/m 3), and BC (1.12; 0.94-1.34 per 0.5 × 10 -5m -1), and a negative association with O 3 (0.74; 0.58-0.94 per 10 µg/m 3). Associations of PM 2.5, NO 2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM 2.5 remained robust when adjusted for NO 2 (1.24; 0.95-1.62) or BC (1.28; 0.96-1.71), whereas associations with NO 2 or BC attenuated to null. O 3 associations remained negative, but no longer statistically significant in models with PM 2.5. We detected suggestive positive associations with the potassium component of PM 2.5. CONCLUSION: Long-term exposure to PM 2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality

Long-term air pollution exposure and Parkinson's disease mortality in a large pooled European cohort: An ELAPSE study

Background: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson's Disease (PD) remains limited. Objective: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts. Methods: Within the project ‘Effects of Low-Level Air Pollution: A Study in Europe’ (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (O3), as well as 8 PM2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders. Results: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM2.5 (hazard ratio per 5 µg/m3: 1.25; 95% confidence interval: 1.01–1.55), NO2 (1.13; 0.95–1.34 per 10 µg/m3), and BC (1.12; 0.94–1.34 per 0.5 × 10-5m-1), and a negative association with O3 (0.74; 0.58–0.94 per 10 µg/m3). Associations of PM2.5, NO2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM2.5 remained robust when adjusted for NO2 (1.24; 0.95–1.62) or BC (1.28; 0.96–1.71), whereas associations with NO2 or BC attenuated to null. O3 associations remained negative, but no longer statistically significant in models with PM2.5. We detected suggestive positive associations with the potassium component of PM2.5. Conclusion: Long-term exposure to PM2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality

Restricted exposure of mice to primer pheromones coincident with prolactin surges blocks pregnancy by changing hypothalamic dopamine release

Exposure of recently mated female mice to strange male urine revealed that exposure for 8 h was sufficient to produce pregnancy block providing exposure is for two 4-h periods coincident with prolactin surges. Exposure for 8 h between prolactin surges or one 4-h exposure coincident with either the nocturnal or the diurnal prolactin surge was without effect. When bromocriptine, a dopamine agonist, was given coincident with the nocturnal and diurnal prolactin surges, it was equally effective, but the opiate antagonist (naltrexone) administered in a similar manner was without effect. This result indicates that pheromonal action is through excitation of the tuberoinfundibular neurones rather than by inhibition of beta-endorphin neurones. Further evidence for dopamine involvement in pregnancy block is demonstrated by showing DOPA accumulation in the medio-basal hypothalamus following exposure to male urinary pheromones after dihydroxybenzylhydrazine (DHBH) administration, which blocks the enzyme DOPA-decarboxylase. Taken together, this series of experiments provides convincing evidence for the dopamine inhibition of prolactin release being the final pathway for pheromone action in the context of pregnancy block