Interstitial lung diseases (ILD) are characterized by fibrotic scarring of the distal lung parenchyma with remarkably unfavorable prognosis. Here we generated a comprehensive portrait of diverse cell types in distal lung and investigated how their spatial organization is altered in fibrosis. We provide the cloupe files for each individual Visium run which can be visualized using the Loupe browser. Each file also contains additional metadata on community membership and annotated histopathological feature for each visium spot overlaid on top of the H&E stained image.

Interstitial lung diseases (ILD) are characterized by fibrotic scarring of the distal lung parenchyma with remarkably unfavorable prognosis. Here we generated a comprehensive portrait of diverse cell types in distal lung and investigated how their spatial organization is altered in fibrosis. We provide the cloupe files for each individual Visium run which can be visualized using the Loupe browser. Each file also contains additional metadata on community membership and annotated histopathological feature for each visium spot overlaid on top of the H&E stained image.

No description available

No description available

Supplementary materials for "Reduction in sclerotic graft-versus-host-disease after post-transplant cyclophosphamide-based regimen comapared to traditional tacrolimus-based regimens in allogeneic hematopoietic cell transplant recipients: a retrospective cohort study"

Supplementary materials for "Reduction in sclerotic graft-versus-host-disease after post-transplant cyclophosphamide-based regimen comapared to traditional tacrolimus-based regimens in allogeneic hematopoietic cell transplant recipients: a retrospective cohort study"

The kynurenine pathway of tryptophan degradation has been implicated in various diseases, including cancer, neurodegenerative disorders, and infectious diseases. A key branchpoint in this pathway is production of the metabolite 3-hydroxy-kynurenine (3-HK) by the enzyme kynurenine 3-monooxygenase (Kmo). We recently found that administration of exogenous 3-HK promotes survival to Salmonella Typhimurium infection in zebrafish larvae by restricting bacterial expansion in macrophages via a systemic mechanism that targets kainate sensitive glutamate receptor (KAR) ion channels. Here, we show that endogenous production of 3-HK by Kmo, likewise, is required for defense against systemic Salmonella Typhimurium infection in vivo and that loss of endogenous production of 3-HK impairs macrophage microbicial activity, resulting in increased bacterial expansion. Mechanistically, 3-HK acts by antagonizing KARs to promote lysosome acidification and subsequent control of bacterial burden. Finally, we establish a novel link between activity at KARs and lysosomal acidification in macrophages, revealing a novel regulatory role for KARs in promoting macrophage microbicidal activity and a novel mechanism though which 3-HK promotes control of bacterial infection.

Clinical metadata for Klebsiella Blood Stream Infection study

Clinical metadata for Klebsiella Blood Stream Infection study

Huntington’s disease arises from a CAG expansion in the huntingtin gene beyond a critical threshold. Current therapeutics primarily aim to reduce toxicity by lowering levels of mutant HTT mRNA and protein. Genetic data support a role for somatic instability in HTT’s CAG repeat as a driver of age of motor dysfunction onset, but currently, the relationship between instability and HTT lowering remains unexplored. Here, we investigate various HTT-lowering modalities to establish the relationship between HTT lowering and instability in Huntington’s disease knock-in mice. We find that repressing transcription of mutant Htt reduces instability, using genetic and pharmacological approaches. Remarkably, zinc finger proteins that target CAG repeats, but lack a repressive domain, protect from somatic instability despite not reducing HTT mRNA or protein levels. These results suggest that DNA-targeted HTT-lowering treatments may have advantages compared to other HTT-lowering approaches, and that steric blockage of CAG repeats may reduce instability while sparing HTT expression.