Rio de Janeiro State University

About: Rio de Janeiro State University is a education organization based out in Rio de Janeiro, Brazil. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 16631 authors who have published 30919 publications receiving 465753 citations. The organization is also known as: UERJ & Rio de Janeiro State University.

Gender, race and parenthood impact academic productivity during the COVID-19 pandemic: from survey to action

Abstract: While the Coronavirus disease 2019 (COVID-19) pandemic is altering academia dynamics, those juggling remote work and domestic demands – including childcare - have already felt the impacts on productivity. Female authors are facing a decrease in papers submission rates since the beginning of the pandemic period. The reasons for this decline in women productivity need to be further investigated. Here we show the influence of gender, parenthood and race in academics productivity during the pandemic period, based on a survey answered by 3,345 Brazilian academics from various knowledge areas and research institutions. Findings revealed that male academics - especially childless ones - were the least affected group, whereas female academics, especially Black women and mothers, were the most impacted group. This scenario will leave long-term effects on the career progression of the most affected groups. The results presented here are crucial for the development of actions and policies that aim to avoid further deepening the gender gap in science. This particular situation we are facing during the pandemic demands institutional flexibility and academia should foster the discussion about actions to benefit Black scientists and academics with families in the post-pandemic scenario.

Impact of COVID-19 on academic mothers.

Abstract: As daily life grinds to a halt worldwide in response to the coronavirus disease 2019 (COVID-19) pandemic, professionals are adjusting to a new reality of remote working. For many researchers, the release from teaching and administrative activities means more time for independent work. In contrast, parents of young children for whom school has been cancelled are facing uniquely challenging responsibilities. Although academic fathers are not immune to the impacts of confinement, it is traditionally women who carry the heaviest load ([ 1 ][1], [ 2 ][2]). These women risk suffering yet another motherhood penalty. Instead of writing papers, they are likely to devote time to homeschooling children and doing household chores. For those who have not yet leaked from the pipeline ([ 3 ][3]) and are struggling to keep their careers on track, these months of heavier duties may increase the distance between them and their male and childless peers. Gender inequality in science is an urgent issue, and motherhood plays a major role in it ([ 4 ][4]). Recent years have witnessed the emergence of many initiatives that ignited changes toward addressing this problem [e.g., ([ 5 ][5]–[ 8 ][6])]. We cannot allow this pandemic to reverse advances and further deepen the gender gap in science. Policies and actions to mitigate the motherhood penalty can benefit all scientists. Deadlines for grant proposals, reports, and renewal requests must be postponed. Funding agencies should consider creating granting programs designed around the reality of academics with families. By instituting more flexible policies, we can make science fairer for everyone affected by the pandemic. 1. [↵][7]1. L. S. Machado et al ., “Parent in science: The impact of parenthood on the scientific career in Brazil,” Proceedings of the 2nd International Workshop on Gender Equality in Software Engineering (2019), pp. 37–40. 2. [↵][8]1. M. A. Mason et al ., Do Babies Matter?: Gender and Family in the Ivory Tower (Rutgers University Press, New Brunswick, NJ, 2013). 3. [↵][9]1. J. Huang et al ., Proc. Natl. Acad. Sci. U.S.A. 117, 4609 (2020). [OpenUrl][10][Abstract/FREE Full Text][11] 4. [↵][12]1. E. A. Cech, 2. M. Blair-Loy , Proc. Natl. Acad Sci U.S.A. 116, 4182 (2019). [OpenUrl][13][Abstract/FREE Full Text][14] 5. [↵][15]1. M. Mills 1. V. A. Jean et al ., in Gender and the Work-Family Experience, M. Mills, Ed. (Springer, 2015), pp. 291–311. 6. Parent in Science ([www.parentinscience.com][16]). 7. Mothers in Science ([www.mothersinscience.com][17]). 8. [↵][18]Mama Is an Academic ( ). [1]: #ref-1 [2]: #ref-2 [3]: #ref-3 [4]: #ref-4 [5]: #ref-5 [6]: #ref-8 [7]: #xref-ref-1-1 "View reference 1 in text" [8]: #xref-ref-2-1 "View reference 2 in text" [9]: #xref-ref-3-1 "View reference 3 in text" [10]: {openurl}?query=rft.jtitle%253DProc.%2BNatl.%2BAcad.%2BSci.%2BU.S.A.%26rft_id%253Dinfo%253Adoi%252F10.1073%252Fpnas.1914221117%26rft_id%253Dinfo%253Apmid%252F32071248%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [11]: /lookup/ijlink/YTozOntzOjQ6InBhdGgiO3M6MTQ6Ii9sb29rdXAvaWpsaW5rIjtzOjU6InF1ZXJ5IjthOjQ6e3M6ODoibGlua1R5cGUiO3M6NDoiQUJTVCI7czoxMToiam91cm5hbENvZGUiO3M6NDoicG5hcyI7czo1OiJyZXNpZCI7czoxMDoiMTE3LzkvNDYwOSI7czo0OiJhdG9tIjtzOjI0OiIvc2NpLzM2OC82NDkyLzcyNC4xLmF0b20iO31zOjg6ImZyYWdtZW50IjtzOjA6IiI7fQ== [12]: #xref-ref-4-1 "View reference 4 in text" [13]: {openurl}?query=rft.jtitle%253DProc.%2BNatl.%2BAcad%2BSci%2BU.S.A.%26rft_id%253Dinfo%253Adoi%252F10.1073%252Fpnas.1810862116%26rft_id%253Dinfo%253Apmid%252F30782835%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [14]: /lookup/ijlink/YTozOntzOjQ6InBhdGgiO3M6MTQ6Ii9sb29rdXAvaWpsaW5rIjtzOjU6InF1ZXJ5IjthOjQ6e3M6ODoibGlua1R5cGUiO3M6NDoiQUJTVCI7czoxMToiam91cm5hbENvZGUiO3M6NDoicG5hcyI7czo1OiJyZXNpZCI7czoxMToiMTE2LzEwLzQxODIiO3M6NDoiYXRvbSI7czoyNDoiL3NjaS8zNjgvNjQ5Mi83MjQuMS5hdG9tIjt9czo4OiJmcmFnbWVudCI7czowOiIiO30= [15]: #xref-ref-5-1 "View reference 5 in text" [16]: http://www.parentinscience.com [17]: http://www.mothersinscience.com [18]: #xref-ref-8-1 "View reference 8 in text"

Protein restriction during gestation and/or lactation causes adverse transgenerational effects on biometry and glucose metabolism in F1 and F2 progenies of rats.

Abstract: Substantial evidence suggests that poor intrauterine milieu elicited by maternal nutritional disturbance may programme susceptibility in the fetus to later development of chronic diseases, such as obesity, hypertension, cardiovascular disease and diabetes. One of the most interesting features of fetal programming is the evidence from several studies that the consequences may not be limited to the first-generation offspring and that it can be passed transgenerationally. In the present study, female rats (F0) were fed either a normal-protein diet [control diet (C); 19 g of protein/100 g of diet] or a low-protein diet [restricted diet (R); 5 g of protein/100 g of diet]. The offspring were termed according to the period and the types of diet the dams were fed, i.e. CC, RC, CR and RR (first letter indicates the diet during gestation and the second the diet during lactation). At 3 months of age, F1 females were bred to proven males, outside the experiment, to produce F2 offspring. At weaning, F2 offspring were divided by gender. RC1 offspring (with the number indicating the filial generation) were born with low birthweight, but afterwards they had catch-up growth, reaching the weight of the CC1 offspring. The increased glycaemia in RC1 offspring was associated with insulin resistance. CR1 and RR1 offspring had impaired growth with no changes in glucose metabolism. RC2 offspring had high BM (body mass) at birth, which was sustained over the whole experiment in male offspring. The F2 generation had more alteration in glucose metabolism than the F1 generation. CR2 and RC2 offspring had hyperglycaemia accompanied by hyperinsulinaemia and insulin resistance in both genders. CR2 offspring had an increase in body adiposity with hyperleptinaemia. In conclusion, low protein during gestation improves BM, fat mass and growth rate in F1 rats, but has adverse effects on glucose and leptin metabolism, resulting in insulin resistance in adult F1 and F2 offspring. Low protein during lactation has adverse effects on glucose, insulin and leptin metabolism, resulting in insulin resistance in adult F2 offspring. These findings suggest that low protein during gestation and/or lactation can be passed transgenerationally to the second generation.

Lipid droplet formation in leprosy: Toll-like receptor-regulated organelles involved in eicosanoid formation and Mycobacterium leprae pathogenesis

Abstract: A hallmark of LL is the accumulation of Virchow's foamy macrophages. However, the origin and nature of these lipids, as well as their function and contribution to leprosy disease, remain unclear. We herein show that macrophages present in LL dermal lesions are highly positive for ADRP, suggesting that their foamy aspect is at least in part derived from LD (also known as lipid bodies) accumulation induced during ML infection. Indeed, the capacity of ML to induce LD formation was confirmed in vivo via an experimental model of mouse pleurisy and in in vitro studies with human peripheral monocytes and murine peritoneal macrophages. Furthermore, infected cells were shown to propagate LD induction to uninfected, neighboring cells by generating a paracrine signal, for which TLR2 and TLR6 were demonstrated to be essential. However, TLR2 and TLR6 deletions affected LD formation in bacterium-bearing cells only partially, suggesting the involvement of alternative receptors of the innate immune response besides TLR2/6 for ML recognition by macrophages. Finally, a direct correlation between LD formation and PGE(2) production was observed, indicating that ML-induced LDs constitute intracellular sites for eicosanoid synthesis and that foamy cells may be critical regulators in subverting the immune response in leprosy.