title: Transcriptomic Hallmarks of Mortality Reveal Universal and Specific Mechanisms of Aging, Chronic Disease, and Rejuvenation

status: Public on Feb 23 2026

first: Alexander

last: Tyshkovskiy

state: Massachusetts

address: 77 Avenue Louis Pasteur

institute: Brigham & Women's Hospital, Harvard Medical School


title: Integrative transcriptomic analysis uncovers the miRNA-centric regulation of Japanese encephalitis virus infection in porcine trophoblast cells [miRNA-Seq]

status: Public on Feb 09 2026

city: Yangzhou

first: Juan

last: Yang

address: 大学南路88号

department: College of Veterinary Medicine

country: China

institute: Yangzhou University

type: Non-coding RNA profiling by high throughput sequencing

summary: To characterize porcine placental miRNAs, we performed small RNA-seq experiments using porcine placental tissues and the porcine placental trophoblast cell line pTr. To investigate the intracellular responses of pTr cells following JEV infection, RNA-seq and small RNA-seq experiments were conducted on pTr cells with or without JEV infection.

overall_design: We collected placental samples from first - parity naturally delivered Duroc gilts, pTr cell samples under normal culture conditions, and pTr cell samples at 24 and 48 hours post - infection with JEV as well as non - infected samples. Two replicates per sample were used for RNA-seq and small RNA-seq experiments.

first: Jiayao

last: Jiang

first: Jiajia

last: Gong

first: Shuai

last: Chen

first: Ming-an

last: Sun


title: Promoter Capture Hi-C performed on human Type 3 Innate Lymphoid Cells (ILC3s)

status: Public on Jan 28 2026

city: London

first: Mikhail

last: Spivakov

address: Du Cane Road

country: United Kingdom

institute: MRC London Institute of Medical Sciences

summary: This promoter capture Hi-C data in tonsil-derived ILC3 cells accompanies the manuscript: "High-resolution promoter interaction analysis implicates genes involved in activation of type 3 innate lymphoid cells in immune disease risk" (Malysheva/Ray-Jones/Lakes et al., Nat Gen 2026)

overall_design: Human ILC3s were isolated from tonsillectomies of three children and promoter capture Hi-C was performed. Libraries were sequenced using paired-end NGS and chromatin interactions were called using CHiCAGO.

first: Valeriya

last: Malysheva

first: Helen

last: Ray-Jones

first: David

last: Ohayon

middle: F

last: Smith

first: Stephen

last: Waggoner


title: Ontogeny-independent expression of LPCAT2 in granuloma macrophages during experimental visceral leishmaniasis [Spatial Transcriptomics]

city: York

first: Paul

middle: M

last: Kaye

state: North Yorkshire

address: University of York, Heslington

institute: Hull York Medical School, University of York

summary: Granulomas are organized inflammatory lesions that form in response to persistent stimuli such as infections. Murine infection with Leishmania donovani results in the formation of granulomas around infected Kupffer cells in the liver and serves as a well-defined model of immune granuloma formation. The formation and resolution of granulomatous inflammation requires dynamic shifts in immune cell activation states, imposing significant metabolic demands. As mediators of energy homeostasis and cell signaling, lipids and lipid metabolism play a key role in regulating immune cell function during inflammation and the response to infection. However, the extent to which alterations in lipids are spatially linked to altered immune cell transcription has yet to be resolved. In this study, we performed a multimodal imaging analysis combining MALDI mass spectrometry, spatial and single cell transcriptomics, proteomics of flow-sorted macrophages and histopathology of L. donovani induced hepatic granulomas. Using this spatially-integrated approach, we identified LPCAT2-mediated membrane re-modelling of myeloid cells as a novel feature of these granulomas. Our study provides new insights into local immunometabolic changes associated with granuloma formation and macrophage activation.

overall_design: Adult female C57BL/6J mice were maintained and bred at the University of York, UK. The mice were housed in ventilated cages under specified pathogen-free conditions with access to food and water ad libitum. Identification of the mouse colony was confirmed through genetic profiling of microsatellite markers, verifying C57BL/6J genetic background with minor variations at 3 markers. Healthy (6-8 week old females) were infected intravenously with 3x107 amastigotes of the Ethiopian LV9 strain of Leishmania donovani to establish visceral infection. At 28 days post-infection, mice were euthanized by CO2 inhalation followed by cervical dislocation according to Home Office regulations. Livers were harvested after euthanization and the major lobe cut and snap-frozen in liquid nitrogen while bathed in isopenane and then kept in -80 degrees until used. For spatial gene expression, 4 infected and 4 uninfected liver sections from individual mice were processed using 10x Visium.

first: Shoumit

last: Dey

first: Jian-Hua

last: Cao

first: Benjamin

last: Balluff

first: Gaia

last: Mazza

last: Ashwin

first: Lesley

last: Gilbert

first: Sally

last: James

first: Adam

middle: A

last: Dowle

first: Grant

last: Calder

first: Nidhi

middle: S

first: Peter

last: O'Toole

first: Ron

last: Heeren