Injury to the vertebrate brain causes neuroinflammation, characterized in part by increases in prostaglandins. In rodents and songbirds, brain injury also induces the transcription and translation of aromatase in reactive astrocytes around the site of damage. Interestingly, this induction is more rapid in female zebra finches relative to males. Induced aromatization is neuroprotective, as inhibition of aromatase and estrogen replacement, increases and decreases the extent of damage, respectively. Although the consequences of induced astrocytic aromatization are intensely studied, little is known about what factors induce aromatase. Inflammation is sufficient to induce astrocytic aromatase suggesting that the link between inflammation and aromatase expression may be causal. To test this hypothesis, adult male and female zebra finches received bilateral mechanical injuries through which either the cyclooxygenase (COX)-1/2 inhibitor indomethacin or vehicle was administered into contralateral hemispheres. Subjects were killed either 6 or 24 hours after injury. In both sexes, an enzyme immunoassay for prostaglandin E2 (PGE2) revealed that indomethacin decreased PGE2 relative to the contralateral hemisphere at both time points, suggesting that the dose and mode of administration used were successful in affecting neuroinflammation locally. Indomethacin reduced aromatase expression and 17β-estradiol (E2) content at 6 hours but not 24 hours following injury in females. However, in males, the inhibitory effect of indomethacin on aromatase and E2 was apparent at 24 but not 6 hours after treatment. These data suggest that COX activity, perhaps via consequent prostaglandin secretion, may induce aromatase expression and central E2, an effect that is detectable in temporally distinct patterns between sexes.
Objective:To determine if maintaining continuity in research topic and method from early to late career yields a greater likelihood of physician-scientists’ research-career success i.e. achieving research independence and producing impactful publications.Methods:To explore the impact of maintaining continuity in research, 108 2000-2010 neurology residency graduates from former Medical Scientist Training Programs at the highest NINDS and NIH funded institutions were identified. Through comparison of Ph.D. dissertations with post-graduate work, research continuity was deemed present if there was evidence of continuity in research topic and method. With publicly available SCOPUS, PubMed, and NIH RePORT data, the correlation that degree of continuity had with h-indices, number of grants awarded, and R01 acquisition was examined.Results:Nearly half of the graduates were classified as non-continuous (45%), less than a quarter classified as somewhat continuous (22%), and roughly a third classified as very continuous (32%). The data demonstrated that research continuity increased the ability to acquire a R01, with 83% percent of R01 and/or R21 recipients having very continuous research. Very continuous graduates also had higher median number of grants received (2 [IQR: 1-3]) and a higher median h-index (17 [IQR: 10.5-20]) compared to the somewhat continuous and non-continuous groups.Conclusions:This study highlights research continuity as an important and modifiable variable during the training period of physician-scientists and one that may improve their career success and promote greater retention within the workforce.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.