Julian E. is a Reporter at The New York Times. He specializes in intelligence and national security reporting, with a strong focus on biology, life sciences, ecology, zoology, and veterinary topics. His work has been featured in prominent publications such as Nature Portfolio, Foreign Policy, and The Atlantic.
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Julian E.'s coverage heavily leans towards government, politics, and world affairs with a focus on evolving stories and breaking news in international relations, espionage, and geopolitical developments. Given this focus, Julian is likely to be receptive to pitches from experts who can provide insights into current geopolitical events or offer analysis on the evolving political landscape of countries like Russia, Ukraine, China, North Korea as well as their relationships with other nations such as the United States.
Given the prevalence of breaking news in Julian's coverage attributes suggests that he may be interested in receiving timely commentary or insider perspectives related to unfolding international incidents or diplomatic negotiations involving major global powers.
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By: Julián E., Marcileia, Cristopher, Victor, Eduardo, Tinajero, Verdugo, Zanatta
Chemical reactor design has traditionally relied on human expertise. Here, the authors present Reac-Discovery, an AI-driven platform that designs, validates, fabricates and optimizes 3D-printed catalytic reactors.
By: Oster, George, Hassinger, David G., Rangamani, Drubin, Padmini, Julian E.
A critical step in cellular-trafficking pathways is the budding of membranes by protein coats, which recent experiments have demonstrated can be in...
By: Victor Phillip Dahdaleh, Marc-Emmanuel, José Maria, José Manuel, Tor Vergata, Jèssica Latorre, Josep Trueta, Harry Perkins
By: James B., Julian E., Vanessa, Carmen R. B.
Species risk to climate change depends in part on their capacity to evolve. Here authors show that the microclimates that native bees occupy in their nests shapes the way tolerance to heat evolves and species corresponding sensitivity to warming.
By: David, George C., Abhay K., Rachel, Julian E., Scott M., Bobustuc, Das, Malley
Purpose Galectin-3 (Gal-3), a multifunctional β-galactoside-binding lectin, is more highly expressed in atypical and anaplastic meningioma subtypes than in normal brain tissue. The mechanism(s) by which Gal-3 may contribute to the aggressive growth of these tumors remains unclear. Methods We evaluated the effects of the Gal-3 inhibitor TD139 combined with either low-intensity direct current electrostimulation (DCES) on meningioma cells in a human co-culture model, or non-invasive transcranial direct current stimulation (tDCS) in an orthotopic preclinical model. Results In vitro, DCES treatment modulated the expression of human leukocyte antigen (HLA) class I and II molecules, which may influence T cell–tumor cell interactions. Gal-3 was found to activate microglia and promote the differentiation of CD4(+) T cells toward Th2 and Treg phenotypes. Treatment with an immunomodulatory dose of DCES, followed by TD139, induced anaplastic meningioma cell death in a human co-culture model without affecting neurons. In the orthotopic allograft preclinical model, treatment with TD139 and tDCS, administered 7 times over 14 days, significantly reduced tumor growth. Survival of tumor-bearing mice treated with TD139 and tDCS was significantly higher than that of untreated controls or mice treated with tDCS or TD139 alone. This combination treatment was also associated with a significant decrease in the meningioma-associated marker NDRG4 and the proliferation marker Ki-67. Conclusion The results indicate that combining Gal-3 inhibitors with direct current stimulation has potential as an effective treatment modality for aggressive meningiomas.
