We believe in you. Best of luck, @[email protected]
RT @[email protected]
From today, our new publishing model comes into full effect.
Your research can now be published as a Reviewed Preprint, with nuanced, high-quality public peer reviews and new eLife assessments.
Learn more: https://elifesciences.org/inside-elife/741dbe4d?utm_source=twitter&utm_medium=social&utm_campaign=organic
π¦π: https://twitter.com/eLife/status/1620418700464754688

eLifeβs New Model: Open for submissions
All papers reviewed by eLife as part of our new model will now be published as Reviewed Preprints.
eLifeRT @[email protected]
π¨Hiring alert for a new #ELISIR scholar π¨
From outstanding #PhD straight to independent #GroupLeader in Lausanne, Switzerland! Conduct research in #LifeSciences - 2023 call prioritizes theoretical and computational biology
Nominations + applications πhttps://go.epfl.ch/ELISIR
π¦π: https://twitter.com/epflSV/status/1618906939030921216

Christoph Feest on Twitter
βπ still open π
Our call "Principal Investigators in AI for Health"
Unique embedding β
Excellent colleagues β
Supportive environment β
Amazing data sets β
Competitive package β
All year cycling π΄ and mountains nearby π§
Ad closes 22 Jan, midnight; #staycuriousβ
TwitterRT @[email protected]
Thrilled to kick off the holiday season with a new paper from the lab! Out in @[email protected] today, we explore an unexpected function of terminally exhausted T cells and their contribution to the immunosuppressive tumor microenvironment. π§΅ 1/ https://www.nature.com/articles/s41590-022-01379-9
π¦π: https://twitter.com/DelgoffeLab/status/1605606197960351745

Hypoxia drives CD39-dependent suppressor function in exhausted T cells to limit antitumor immunity - Nature Immunology
Exhausted CD8+ T cells with diminished effector functions accumulate in tumors. Here, the authors show that hypoxia induces a suppressive phenotype in exhausted T cells and that interfering with hypoxia-mediated CD39 expression limits immunosuppression in the tumor and augments immunotherapy, resulting in arrest of tumor growth.
NatureRT @[email protected]
Authored by Andrew G. Soerens et al, we show that #Tcells are capable of proliferating in response to iterative stimulation for over 10yrs! And produce enough progeny to occupy a volume 30,000x the Earth's volume! @[email protected] https://www.nature.com/articles/s41586-022-05626-9
π¦π: https://twitter.com/Masopust_Vezys/status/1615785991154843670

Functional T cells are capable of supernumerary cell division and longevity - Nature
Through iterative cycles of viral challenge and rechallenge over ten years, mouse T cells are demonstrated to have essentially infinite potential for population expansion and longevity without malignant transformation or loss of functional competence.
NatureRT @[email protected]
Extremely happy to share our last paper in @[email protected] with the community! Big team effort, congrats and a huge thank you to all authors, it was a pleasure to work with all of you on this! π₯³π₯³π₯³ #immunogenomics #TME #brain_metastasis https://twitter.com/johanna_a_joyce/status/1615376628317650949
π¦π: https://twitter.com/aalvarezprado/status/1615383584436633603

Johanna Joyce on Twitter
βHow do cancer cells sculpt their tumor microenvironment??π€
We analyzed brain metastases, from lung or breast primary cancers - and associated w/ different genetic alterations, to reveal distinct immune cell landscapes and phenotypes β¬
https://t.co/b4j2P5phI9
#openaccess #TMEβ
TwitterRT @[email protected]
Are you interested in the intersection of chemogenomics, machine learning and drug discovery? Our new review, "Targeting Trypanosomes: How Chemogenomics and Artificial Intelligence Can Guide Drug Discovery," is sure to get your attention!
https://portlandpress.com/biochemsoctrans/article-abstract/doi/10.1042/BST20220618/232416/Targeting-trypanosomes-how-chemogenomics-and?redirectedFrom=fulltext
π¦π: https://twitter.com/leitouran/status/1612586065763745792
Targeting trypanosomes: how chemogenomics and artificial intelligence can guide drug discovery
Trypanosomatids are protozoan parasites that cause human and animal neglected diseases. Despite global efforts, effective treatments are still much needed. Phenotypic screens have provided several chemical leads for drug discovery, but the mechanism of action for many of these chemicals is currently unknown. Recently, chemogenomic screens assessing the susceptibility or resistance of parasites carrying genome-wide modifications started to define the mechanism of action of drugs at large scale. In this review, we discuss how genomics is being used for drug discovery in trypanosomatids, how integration of chemical and genomics data from these and other organisms has guided prioritisations of candidate therapeutic targets and additional chemical starting points, and how these data can fuel the expansion of drug discovery pipelines into the era of artificial intelligence.
Portland PressRT @[email protected]
After more than 2 years of work, I am happy to share our latest preprint on CellCharter, a computational framework to identify and study cellular niches in large-scale spatial transcriptomics and proteomics data π§΅ 1/12
https://www.biorxiv.org/content/10.1101/2023.01.10.523386v1
π¦π: https://twitter.com/MarcoVarrone/status/1613463315547672581