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International audience; Background: COVID-19 triggered an unprecedented crisis affecting society at every level. Research in pediatric and congenital cardiology is currently in full development and may have been disrupted. The aim of the study was to determine the impact of COVID-19 on pediatric and congenital cardiology clinical research and to analyze decision-making and adaptation processes, from a panel of ongoing academic and industry-sponsored research at the time of the pandemic.Methods: This observational study was carried out in April 2020, from a CHD clinical research network involving five tertiary care pediatric and congenital cardiology centers. Investigators and clinical research assistants from each participating research center completed an online survey questionnaire, and each principal investigator underwent a 1-h web-based videoconference interview.Results: A total of 34 study questionnaires were collected, reporting that 18 studies were totally suspended. Upon the investigator's decision, after discussion on ethical issues and with facilitating support from health authorities, 16 studies were resumed. The rate of study suspension in interventional research (53%) was similar to that in non-interventional research (56%). Logistical problems were predominantly reported in both continued and suspended trials. Research protocols were adapted, largely thanks to telemedicine, which in some cases even improved the course of the study.Conclusion: The impact of the COVID-19 pandemic on clinical research in pediatric and congenital cardiology has been limited by a rapid adaptation of all research structures and an extensive use of telemedicine at all stages of the studies.

Background COVID-19 triggered an unprecedented crisis affecting our society at every level. Clinical research in paediatric and congenital cardiology is currently in full development and may have been disrupted. Aims To determine the impact of COVID-19 in paediatric and congenital cardiology clinical research and to analyse decision-making and adaptation processes, from a panel of on-going academic and industry-sponsored research at the time of the pandemic. Methods This observational study was carried out in April 2020, from a CHD clinical research network involving five tertiary care paediatric and congenital cardiology centres. Investigators and clinical research assistants from each participating research centre filled in an online survey questionnaire, and each principal investigator underwent a one-hour web-based videoconference interview. Results From a total of 34 study questionnaires and 288 enrolled patients at the time of the pandemic, 18 studies were declared as totally suspended. Upon investigator's decision, after discussion on ethical issues and with facilitating support from health authorities, 16 studies were resumed. The rate of study suspension in interventional research (53%) was similar to non-interventional research (56%). Logistical problems were predominantly reported in both continued and suspended trials. Research protocols were adapted, largely thanks to telemedicine, which in some cases even improved the course of the study. Conclusions The impact of the COVID-19 pandemic on clinical research in paediatric and congenital cardiology has been limited by a rapid adaptation of all research structures and an extensive use of telemedicine at all stages of the studies.

Formation of colonies from mice bone marrow progenitors of macrophages and granulocytes in methylcellulose culture was induced by an inflammatory pleural exudate obtained from mice injected with dextran. Mitogenic activity of this acute inflammatory exudate was compared with that of colony stimulating factor (CSF). It was found that colony and cluster counts, during 10 days of culture, were similar with the two types of stimulating factors. When used at the same dose, exudate was less active than CSF. It was concluded that inflammatory exudate showed an activity similar to that of CSF but contained a smaller amount of stimulating factor. Further cytochemical studies are necessary to specify whether or not the two factors induced the same type of colonies (monocytic or granulocytic).

It has been shown that rat peritoneal macrophages in culture were modified following treatment with inflammatory cell-free exudates induced by intrapleural injection of dextran1–2. The main results are summarized in Table 43.1. They were obtained with non-inbred (Sprague-Dawley), and inbred strain of rats (Lewis, WAG). A similar effect, although less intense, was found following treatment of mouse peritoneal macrophages with rat exudates. Similar results were obtained by Wynne et al. 3 using exudates obtained from chronic inflammatory lesions. The induction of DNA synthesis and division of macrophages in culture were related to the release of a mitogenic factor in these particular inflammatory exudates.

Acute non immunological inflammatory pleural exudates provoked by four different irritants and collected 4 hours later have been shown to be capable of stimulating DNA synthesis, in rat peritoneal macrophages in culture. It is postulated that a mitogenic factor, "Inflammatory Mitogenic Factor for Macrophages" IMF (M), could be responsible for this phenomenon. There may be a correlation between the protein concentration of the exudates and its mitogenic activity.

Rat macrophages in culture are induced to synthesize DNA when incubated with Dextran pleural exudate. Previous or simultaneous in vitro treatment with dexamethasone phosphate used at different concentrations was able to inhibit or decrease that induction. This effect could represent a new aspect of the influence of corticosteroids in the inflammatory process.

An inflammatory exudate obtained in Swiss mice 3 hours after intrapleural injection of dextran was able to increase the number of cultivated peritoneal macrophages in S phase. This exudate was also able to stimulate the formation of colonies from mice bone marrow progenitors of macrophages and granulocytes in methylcellulose culture. The stimulating activity of this acute inflammatory exudate was compared with that of colony stimulating factor (GM.CSF). The qualitative and quantitative results showed that the biological activity of the mitogenic factor of this inflammatory exudate, inflammatory mitogenic factor (IMF) was very close to GM.CSF at optimal concentration, but when used at the same concentration, the exudate was less active than GM.CSF. A stimulating activity was also found with another inflammatory pleural exudate induced by calcium pyrophosphate. The comparative kinetics of the action of the two exudates on CFUc appeared alike but the rise was earlier with calcium pyrophosphate. These results suggest the release of a growth factor for monocyte-macrophage in different acute inflammatory exudates.