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Rajendran, L.

Publications and source records attributed to Rajendran, L..

2 recordsLinked to original sources

Woman Authorship in Pre-print Versus Peer-Reviewed Oral Health-Related Publications: A Two-Year Observational Study

ObjectivesWomen in oral health science face similar societal issues and challenges as those in other STEMM careers, and gender disparities continue to exist as evidenced by fewer women represented as first and last authors in scientific publications. Pre-prints may serve as a conduit to immediately disseminating ones work, bypassing the arduous peer review process and its associated inherent biases. Therefore, the purpose of this study was to 1] compare the gender of first and last authors in pre-print versus peer reviewed publications, 2] examine the composition of first and last author pairs as stratified by publication type, and 3] examine the correlation between woman authorship and institutional geographic location and publication metrics stratified by publication type. MethodsThe keyword "oral health" was used to search for publications in BioRxiv and Pubmed in the years 2018 and 2019. Gender of first and last authors were determined, and its frequency was considered as the primary outcome. Additionally, the geographic location of the authors associated institution and publication metrics measured by Altmetrics score were extracted. Data was descriptively summarized by frequencies and percentages. Chi-square analysis was conducted for categorical variables which included the relationship between gender and publication type as well as gender and region of authors associated institution. Binomial regression analysis was conducted to analyze the relationship between gender and Altmetrics. ResultsWoman first authors comprised 40.3% of pre-prints and 64.5% of peer reviewed publications [p<0.05]. Woman last authors comprised 31.3% of pre-prints and 61.5% of peer reviewed publications [p<0.05]. When analyzing the relationships between first and last author, the Man-Man pairing represented 47.7% of the pre-print publications and the Woman-Woman pairing comprised a majority of the of the peer review publications at 47.5%. All results were statistically significant with a p-value <0.05. No significant correlation was found between region of institution or Altmetrics and gender of first or last authors [p>0.05]. ConclusionFor the first time in oral health science, it was found that women show higher representation as first and last author positions in peer reviewed publications versus pre-prints.

scientific communication and education↗

Nutrient signaling pathways regulate amyloid clearance and synaptic loss in Alzheimer's disease

Extra-cellular accumulation of Amyloid-{beta} (A{beta}) plaques is causatively associated with Alzheimers disease (AD). However, mechanisms that mediate the pre-pathological state of amyloid plaque formation remain elusive. Here, using paired RNAi and kinase inhibitor screens, we discovered that AKT-mediated insulin/nutrient signaling suppresses lysosomal clearance of A{beta} and promotes amyloid formation. This mechanism is cell-autonomous and functions in multiple systems, including iPSC-derived human neurons and in vivo. Nutrient signaling regulates amyloid formation via distinct lysosomal functional mechanisms, while enhanced amino acid signaling promotes amyloid formation by transcriptionally suppressing lysosome biogenesis, and high intracellular cholesterol levels suppress lysosomal clearance of amyloid by increasing the number of non-functional lysosomes. The nutrient signaling pathway, present in both neurons and microglia, regulates lysosomal clearance of amyloid and microglia mediated synapse loss, both in vitro and in vivo. Clinically, older hyperlipidemic patients showed less synapse loss through microglia and performed better in cognitive tests. Thus, our results reveal a bi-partite cellular quality control system regulated by the insulinnutrient signaling that in neurons regulates A{beta} peptide clearance and in microglia regulates synaptic loss, both processes causally associated with AD. Our results also caution against reducing amyloid through such processes as this might also result in synapse loss.

neuroscience↗